The atherothrombotic cascade
Eight ordered steps from lipid entry to myocardial injury. Tap a step — or let it auto-advance — to see what accumulates there.
Lipid retention & oxidation
ApoB-lipoprotein retention in the subendothelial intima and their oxidative modification — the initiating substrate of atherogenesis.
Every molecule in each step — refs, trials, mechanism and a confidence dot per row.◆ druggable · ✦ genetic
Lipid retention & oxidation
Lipid entry/oxidation256| Molecule | Type | Conf. | Refs | Trials | Evidence | Mechanism |
|---|---|---|---|---|---|---|
| LDL cholesterol | lipoprotein | 60 | 6 | — | LDL accumulation in the arterial intima is the initiating substrate of atherosclerotic plaque formation. | |
| Oxidized LDL | lipoprotein | 60 | 2 | — | Oxidized LDL drives plaque formation, inflammation, and endothelial dysfunction in atherothrombotic disease. | |
| HDL | lipoprotein | 60 | — | — | HDL exerts atheroprotective effects via reverse cholesterol transport, antioxidant activity, and endothelial stabilization. | |
| Apolipoprotein BAPOB | protein | 49 | 3 | ✦◆ | ApoB-containing lipoproteins are retained in the subendothelium and oxidatively modified, initiating atherogenesis. | |
| Lipoprotein(a)LPA | lipoprotein | 46 | 19 | ✦◆ | Lipoprotein(a) is an ApoB-containing lipoprotein retained in the subendothelial intima where it undergoes oxidative modification; its apo(a) moiety confers inde | |
| Apolipoprotein A-IAPOA1 | protein | 30 | 1 | ◆ | ApoA-I is the major HDL component mediating reverse cholesterol transport and endothelial protective effects; reduced levels indicate atherosclerotic burden. | |
| Apolipoprotein EAPOE | protein | 26 | — | ✦◆ | Apolipoprotein E is a lipoprotein structural protein and receptor ligand whose genetic polymorphisms influence LDL metabolism, lipoprotein retention, and athero | |
| PCSK9PCSK9 | protein | 25 | 20 | ✦◆ | PCSK9 regulates LDL-receptor degradation, controlling LDL-C levels and subendothelial lipid retention underlying atherosclerosis. | |
| Lysophosphatidylcholine | lipid | 23 | — | — | Lysophosphatidylcholine, a bioactive lipid species derived from lipoprotein remodeling, promotes atherosclerosis and altered lipid homeostasis in Type 1 MI. | |
| Lectin-like Oxidized LDL Receptor 1 | protein | 22 | — | — | LOX-1 mediates uptake of oxidized LDL by endothelial cells and macrophages, fueling plaque lipid accumulation and inflammation. | |
| Very-Low-Density Lipoprotein | lipoprotein | 21 | — | — | VLDL, an apoB-containing atherogenic lipoprotein, accumulates in the arterial intima where it undergoes oxidative modification, initiating atherosclerotic plaqu | |
| Phosphatidylcholine | lipid | 18 | — | — | Phosphatidylcholine species composition of lipoproteins and plaques reflects atherogenesis severity and plaque lipid core character. | |
| LDL ReceptorLDLR | gene | 17 | 3 | ✦◆ | LDLR mediates LDL endocytosis; mutations impair LDL clearance, driving lipid retention and accelerated atherogenesis. | |
| Sphingomyelin | lipid | 17 | — | — | Sphingomyelin alters LDL aggregation susceptibility and membrane integrity, contributing to lipid retention and oxidative modification in the atherosclerotic le | |
| HDL cholesterol | lipoprotein | 16 | 1 | — | HDL removes cholesterol and phospholipid hydroperoxides from lesions, opposing atherosclerotic lipid accumulation. | |
| Ceramide | lipid | 16 | — | — | Ceramide is a pro-atherogenic bioactive lipid that drives altered lipid metabolism, LDL aggregation, foam-cell formation and atherosclerotic plaque progression. | |
| Triglycerides | lipid | 15 | 2 | — | Elevated triglycerides promote atherosclerotic lipid deposition and dysfunctional lipoprotein remodeling. | |
| Trimethylamine N-oxide | metabolite | 13 | — | — | TMAO promotes lipid oxidation, plaque inflammation and destabilization, increasing atherothrombotic rupture and thrombotic risk. | |
| Ceramides | lipid | 10 | — | — | Ceramide elevation is a biomarker of atherosclerotic disease progression and cardiometabolic lipid stress in acute MI. | |
| Apolipoprotein C3APOC3 | protein | 9 | — | ◆ | ApoC3 on atherogenic remnants attenuates clearance and intensifies subendothelial lipid retention, plaque inflammation, and rupture risk in Type 1 MI. | |
| Paraoxonase 1PON1 | protein | 9 | — | ✦◆ | PON1 is an HDL-associated esterase that hydrolyzes oxidized phospholipids in LDL, preventing lipid-core accumulation and plaque inflammation. | |
| Lipoprotein lipaseLPL | protein | 8 | — | ✦◆ | Rate-limiting enzyme hydrolyzing triglycerides in atherogenic lipoproteins, regulated by ANGPTL inhibitors. | |
| Oxidized Phospholipids | lipid | 8 | — | — | Oxidized phospholipids generated from atherosclerotic lipid oxidation drive plaque inflammation and vascular cell activation in atherothrombotic cascade. | |
| triglyceride | metabolite | 7 | 1 | — | Elevated triglycerides reflect accumulation of atherogenic lipoproteins in the intima, driving oxidative lipid modification and atherosclerotic plaque formation | |
| Cholesterol | metabolite | 7 | — | — | Cholesterol and atherogenic lipoprotein-associated cholesterol drive intimal retention, foam cell formation, inflammasome activation, and plaque destabilization | |
| Sortilin 1SORT1 | gene | 7 | — | ✦◆ | Hepatic lipid-sorter regulating LDL metabolism and ApoB lipoprotein retention, driving atherothrombotic MI risk. | |
| Apolipoprotein C-IAPOC1 | protein | 6 | — | ✦◆ | ApoC-I regulates lipoprotein metabolism and is associated with both retained lipid burden and systemic inflammation in atherosclerosis. | |
| Intermediate-density lipoprotein | lipoprotein | 6 | — | — | IDL is retained in the arterial intima and undergoes oxidative modification, seeding atherosclerotic plaque formation. | |
| Lipase A, lysosomal acid typeLIPA | protein | 6 | — | ✦◆ | LIPA expressed in monocytes and macrophages catalyzes cholesterol-ester hydrolysis in the atherosclerotic lesion, exacerbating lipid retention and inflammation. | |
| Phosphatidylinositol | lipid | 6 | — | — | Phosphatidylinositol is a structural lipoprotein lipid altered by oxidative stress; reduced levels in MI-prone and vascular disease states mark lipid peroxidati | |
| PPARGPPARG | gene | 6 | — | ◆ | PPARG promotes reverse cholesterol transport and resolves post-MI inflammation, opposing atherosclerotic lipid accumulation. | |
| Triacylglycerols | lipid | 6 | — | — | Elevated triacylglycerols in plaque and thrombus mark atherosclerotic burden, plaque vulnerability, and thrombotic risk. | |
| Total cholesterol | lipid | 5 | 1 | — | Circulating total cholesterol, particularly in apoB-lipoproteins, drives subendothelial lipid retention and plaque formation. | |
| Angiopoietin-like 3ANGPTL3 | protein | 5 | — | ◆ | ANGPTL3 reduces triglyceride-rich lipoprotein atherogenicity and predicts adverse atherosclerotic events. | |
| Angiopoietin-like 4ANGPTL4 | protein | 5 | — | ◆ | ANGPTL4 inhibits lipoprotein lipase, impairing ApoB-lipoprotein clearance and promoting atherogenic dyslipidemia and lipid retention in Type 1 MI. | |
| Cholesteryl esters | lipid | 5 | — | — | Cholesteryl esters accumulate in foam cells and atherogenic lipoproteins, driving plaque formation and remodeling post-MI. | |
| lysophosphatidylethanolamine | lipid | 5 | — | — | Lysophosphatidylethanolamine dysregulation in monocytes and plaques associates with CAD risk, plaque burden, and acute coronary events. | |
| Non-HDL cholesterol | lipid | 5 | — | — | Non-HDL cholesterol quantifies circulating atherogenic lipoproteins driving subendothelial lipid retention and oxidative modification. | |
| Plasmalogens | lipid | 5 | — | — | Plasmalogens are atheroprotective alkenylphospholipids whose depletion associates with atherosclerotic plaque instability and acute coronary syndrome. | |
| Small dense LDL | lipoprotein | 5 | — | — | Small dense LDL particles are highly atherogenic, readily retained in the arterial intima, and oxidized to promote atherosclerotic plaque initiation. | |
| Fatty acids | lipid | 4 | 6 | — | Fatty acid composition and metabolism influence lipoprotein atherogenicity and vascular endothelial function in atherothrombotic disease. | |
| Cholesteryl ester | lipid | 4 | 1 | — | Cholesteryl esters accumulate in atherosclerotic plaques as the core lipid component, marking lipid-rich plaque burden and cardiovascular risk. | |
| Choline | metabolite | 4 | 1 | — | Dietary and metabolic marker associated with lipid retention, plaque inflammation, and thrombotic MI risk. | |
| Remnant Cholesterol | lipid | 4 | 1 | — | Remnant lipoproteins accumulate in the arterial intima and undergo oxidative modification, initiating atherosclerotic plaque formation. | |
| Triacylglycerol | lipid | 4 | 1 | — | Triacylglycerol-rich lipoproteins are retained in plaque and promote atherogenesis and plaque vulnerability. | |
| Apolipoprotein A-IVAPOA4 | protein | 4 | — | ◆ | Apolipoprotein involved in lipid metabolism and stress-response pathways affecting coronary risk. | |
| ATP-Binding Cassette Transporter A1ABCA1 | gene | 4 | — | ◆ | ABCA1 mediates reverse cholesterol transport and HDL particle biogenesis, reducing atherosclerotic lipid burden. | |
| ATP-Binding Cassette Transporter G1ABCG1 | protein | 4 | — | ◆ | ABCG1 hypermethylation in CHD impairs cholesterol efflux and lipid homeostasis, promoting lipid retention and atherogenesis. | |
| Fatty Acid Binding Protein 4FABP4 | protein | 4 | — | ◆ | Adipocyte fatty acid-binding protein 4 reflects lipid trafficking and plaque instability, predicting atherosclerotic progression and adverse events. | |
| Immunoglobulin M | protein | 4 | — | — | IgM autoantibodies targeting oxidized lipoproteins suppress lipid retention and promote clearance of modified LDL, reducing plaque burden. | |
| Malondialdehyde | metabolite | 3 | 1 | — | MDA is generated by lipid peroxidation and reflects both LDL oxidation and oxidative damage to the endothelial glycocalyx. | |
| Angiopoietin-like 8ANGPTL8 | protein | 3 | — | ◆ | Inhibitor of lipoprotein lipase controlling triglyceride-rich lipoprotein and remnant cholesterol metabolism in dyslipidemia. | |
| Apolipoprotein A-IIAPOA2 | protein | 3 | — | ◆ | An HDL apolipoprotein whose plaque levels and modification state correlate with atherosclerotic progression and plaque destabilization. | |
| Apolipoprotein C-IIAPOC2 | lipoprotein | 3 | — | ◆ | Apolipoprotein C-II modulates triglyceride-rich lipoprotein metabolism and is elevated in acute coronary syndrome. | |
| Apolipoprotein FAPOF | protein | 3 | — | ◆ | APOF modulates HDL-mediated lipid metabolism and LXR-pathway activation, affecting atherosclerotic lipid retention and post-MI remodeling. | |
| CELSR2CELSR2 | gene | 3 | — | ✦◆ | CELSR2 genetic variants regulate lipid retention and atherogenic lipoprotein handling, driving atherosclerotic lesion formation. | |
| Cer(d18:1/18:0) | lipid | 3 | — | — | Cer(d18:1/18:0) amplifies lipid retention and inflammatory signaling in atherosclerotic plaques, predicting adverse thrombotic events. | |
| Ceramide(d18:1/16:0) | lipid | 3 | — | — | Cer(d18:1/16:0) is a bioactive ceramide lipid associated with coronary artery disease severity and acute coronary syndrome prognosis. | |
| Docosahexaenoic acid | lipid | 3 | — | — | Docosahexaenoic acid, an omega-3 polyunsaturated fatty acid, accumulates differentially in stable versus rupture-prone atherosclerotic plaques and correlates wi | |
| Hexosylceramide | lipid | 3 | — | — | Altered hexosylceramide metabolism contributes to atherosclerotic plaque lipotoxicity and post-MI ventricular remodeling. | |
| Immunoglobulin G | protein | 3 | — | — | IgG autoantibodies targeting oxidized LDL form circulating immune complexes that promote plaque inflammation and destabilization. | |
| LysoPC(18:2(9Z,12Z)) | lipid | 3 | — | — | Lysophosphatidylcholine species altered in acute coronary syndrome, marking lipoprotein oxidation and inflammatory lipid-mediator activation. | |
| miR-122 | rna | 3 | — | — | miR-122 dysregulation impairs lipid homeostasis and is elevated early in myocardial infarction, linking to the lipid retention and oxidative modification phase | |
| Oxysterols | lipid | 3 | — | — | Oxysterols are biomarkers and drivers of ApoB-lipoprotein oxidation, the initiating substrate of atherosclerotic plaque formation and destabilization. | |
| palmitic acid | metabolite | 3 | — | — | Palmitic acid elevation reflects disturbed lipid metabolism and inflammatory lipid signaling in acute coronary syndrome. | |
| Palmitoleic acid | metabolite | 3 | — | — | Monounsaturated fatty acid elevated in ACS, reflecting ischemia-associated acylcarnitine dysmetabolism. | |
| Remnant lipoprotein | lipoprotein | 3 | — | — | Remnant lipoproteins are retained and oxidized in the arterial intima, initiating atherosclerotic plaque formation and Type 1 MI risk. | |
| Sphingosine | lipid | 3 | — | — | Sphingosine dysmetabolism contributes to lipid accumulation and oxidative stress in atherosclerotic plaque and myocardial injury. | |
| Triglyceride-rich lipoprotein | lipoprotein | 3 | — | — | Triglyceride-rich lipoprotein accumulation in subendothelium initiates lipid oxidation and atherogenic inflammation driving atherothrombotic MI. | |
| Zinc-Alpha-2-GlycoproteinAZGP1 | protein | 3 | — | ◆ | AZGP1 promotes reverse cholesterol transport and suppresses inflammatory signaling, protecting against atherosclerotic lipid accumulation and plaque inflammatio | |
| Acyl-CoA synthetase long-chain family member 1ACSL1 | gene | 2 | — | ◆ | ACSL1 overexpression in macrophages drives lipid uptake and esterification, promoting foam-cell formation and plaque destabilization. | |
| APODAPOD | gene | 2 | — | ◆ | APOD deficiency impairs HDL-mediated lipid homeostasis and anti-inflammatory signaling, promoting lipid retention and plaque inflammation. | |
| Apolipoprotein A-VAPOA5 | protein | 2 | — | ✦◆ | APOA5 accelerates lipoprotein lipase function, modulating ApoB-lipoprotein clearance and atherogenic dyslipidemia in Type 1 MI. | |
| Apolipoprotein C | lipoprotein | 2 | — | — | Apolipoprotein C mediates lipid metabolism and HDL remodeling; its altered expression during plaque rupture and coronary events reflects changes in lipoprotein | |
| Campesterol | metabolite | 2 | — | — | Campesterol, a plant sterol, is elevated in CAD/MI and reflects altered lipid metabolism and atherogenic lipid retention. | |
| CATCAT | gene | 2 | — | ◆ | CAT dysregulation impairs hydrogen-peroxide clearance, allowing lipid-driven oxidative stress to amplify atherosclerotic lesion progression. | |
| Ceramide (d18:1/24:0) | lipid | 2 | — | — | Ceramide accumulation in atherosclerotic plaques associates with ACS susceptibility and stenosis severity. | |
| Ceramide(d18:1/24:1) | lipid | 2 | — | — | Cer(d18:1/24:1) is a bioactive ceramide lipid associated with coronary artery disease severity and acute coronary syndrome prognosis. | |
| Complement Receptor 1CR1 | protein | 2 | — | ◆ | CR1 modulates complement-dependent oxidized lipoprotein clearance and inflammatory signaling in atherosclerotic plaque. | |
| CYP1B1CYP1B1 | gene | 2 | — | ◆ | CYP1B1 catalyzes oxidative metabolism and lipid peroxidation amplifying atherosclerotic inflammation and lesion progression. | |
| Desialylated LDL | lipoprotein | 2 | — | — | Desialylated LDL is a glycosylation-modified form with reduced clearance and enhanced atherogenic lipoprotein retention in the arterial intima and immune activa | |
| Diacylglycerols | lipid | 2 | — | — | Elevated diacylglycerols in atherosclerotic plaque and thrombus influence lipid-mediated inflammation and platelet activation. | |
| dihydroceramide | lipid | 2 | — | — | Dihydroceramide accumulation correlates with oxidative modification of retained lipoproteins and inflammatory lipid signaling in plaques. | |
| Glutathione peroxidaseGPX1 | protein | 2 | — | ◆ | Glutathione peroxidase limits oxidative modification of retained lipoproteins and protects endothelial function. | |
| Hepatic lipaseLIPC | protein | 2 | — | ◆ | Hepatic lipase remodels lipoprotein composition through triglyceride and phospholipid hydrolysis, influencing atherogenic lipoprotein heterogeneity. | |
| Lysophosphatidylcholine a C17:0 | lipid | 2 | — | — | Lysophosphatidylcholine a C17:0 is an oxidized lipid product characteristic of acute coronary syndrome metabolomic profiles. | |
| lysophosphatidylcholines | lipid | 2 | — | — | Lysophosphatidylcholines are oxidized phospholipid metabolites that promote inflammatory signaling and contribute to plaque destabilization in acute coronary sy | |
| Malondialdehyde-modified LDL | lipoprotein | 2 | — | — | Malondialdehyde-modified LDL is an oxidized ApoB-lipoprotein derivative driving plaque lipid-core accumulation and inflammatory macrophage recruitment. | |
| miR-33 | rna | 2 | — | — | MicroRNA controlling ABCA1 and SREBP-mediated lipid metabolism, modulating lipoprotein retention and atherogenesis initiation. | |
| Oleic acid | lipid | 2 | — | — | Oleic acid dysregulation in ACS-HTN reflects aberrant lipid metabolism and metabolic comorbidity-specific signatures in acute myocardial injury. | |
| Oxidized HDL | lipid | 2 | — | — | Oxidized HDL loses its antiatherogenic properties and promotes foam cell formation and plaque inflammation. | |
| Paraoxonase 3PON3 | protein | 2 | — | ◆ | Antioxidant enzyme reducing oxidative modification of lipoproteins and limiting atherosclerotic lesion progression. | |
| Phosphatidylethanolamines | lipid | 2 | — | — | Phosphatidylethanolamine enrichment in atherosclerotic lipoproteins reflects atherogenic lipid remodeling. | |
| Plasmalogen | lipid | 2 | — | — | Plasmalogens are ether-linked lipids with antioxidant function; their reduction in MI-prone and atherosclerotic vessels marks increased oxidative burden. | |
| Proline/Serine-Rich Coiled-Coil 1PSRC1 | gene | 2 | — | ✦ | A genetic locus influencing atherosclerotic plaque development and MI susceptibility, likely through lipid or metabolic pathways. | |
| Sphingomyelins | lipid | 2 | — | — | Sphingomyelin composition of lipoproteins and atherosclerotic plaques influences lipid-driven atherogenesis. | |
| Superoxide Dismutase 1SOD1 | protein | 2 | — | ◆ | SOD1 catalyzes superoxide dismutation, reducing oxidative stress and preventing LDL oxidation that would otherwise accelerate plaque lipid-core expansion. | |
| Triacylglycerol 52:4 | lipid | 2 | — | — | A specific triacylglycerol species enriched in calcified coronary plaque that contributes to lipid retention and atherogenic progression. | |
| Triglyceride-rich lipoprotein cholesterol | lipoprotein | 2 | — | — | Triglyceride-rich lipoprotein cholesterol is an atherogenic lipoprotein fraction that independently predicts atherosclerotic cardiovascular disease. | |
| Cholesteryl ester transfer proteinCETP | protein | 1 | 1 | ◆ | CETP modulates HDL cholesterol content and ApoB-lipoprotein metabolism, influencing atherosclerotic burden. | |
| Eicosapentaenoic acid | lipid | 1 | 1 | — | Eicosapentaenoic acid, an omega-3 polyunsaturated fatty acid, associates with plaque stability and suppresses thromboxane-driven platelet aggregation. | |
| Vitamin E | metabolite | 1 | 1 | — | Vitamin E depletion reflects oxidative stress during LDL modification and lipid-core pathogenesis in atherosclerotic plaque. | |
| 2-ketobutyric acid | metabolite | 1 | — | — | 2-ketobutyric acid accumulation reflects altered branched-chain amino-acid metabolism and plaque lipotoxicity in ACS. | |
| 4-Cholestenone | lipid | 1 | — | — | Oxidized steroid metabolite indicative of lipoprotein oxidation and prothrombotic lipid environment. | |
| 7-hydroperoxycholesterol | metabolite | 1 | — | — | 7-hydroperoxycholesterol reflects cholesterol oxidation in the atherosclerotic intima and triggers endothelial injury. | |
| 7-Ketocholesterol | lipid | 1 | — | — | Oxidized cholesterol metabolite biomarker for lipid peroxidation, plaque destabilization, and thrombotic MI. | |
| 8-iso-PGF2α | metabolite | 1 | — | — | 8-iso-PGF2α quantifies free-radical-driven lipid peroxidation in atherogenic lipoprotein oxidation and plaque destabilization. | |
| 9(R)-HODE | lipid | 1 | — | — | 9(R)-HODE is an oxidized linoleic acid metabolite reflecting lipid peroxidation and oxidative stress in acute myocardial events. | |
| A4GNTA4GNT | gene | 1 | — | ◆ | A4GNT modulates glycosylation of lipoproteins and immune receptors, influencing oxidative modification and inflammatory responses in atherogenesis. | |
| Abhydrolase domain-containing protein 5ABHD5 | gene | 1 | — | ◆ | ABHD5 modulates lipid catabolism affecting circulating and arterial lipid burden. | |
| Acyl-alkyl-phosphatidylcholine C36:3 | lipid | 1 | — | — | Acyl-alkyl (plasmalogen) phosphatidylcholine composition independently predicts MI risk via altered lipoprotein biology. | |
| ALOX15ALOX15 | protein | 1 | — | ◆ | ALOX15 catalyzes lipoxygenase-mediated oxidation of polyunsaturated lipids, generating oxidized phospholipids and cholesterol oxides in atherosclerotic lesions. | |
| Anti-oxidized LDL antibodies | protein | 1 | — | — | Anti-oxLDL antibodies reflect the extent of lipoprotein oxidative modification, a key atherogenic signal in subendothelial lipid retention. | |
| Apolipoprotein C-IVAPOC4 | protein | 1 | — | ◆ | APOC4 regulates lipoprotein metabolism and lipid composition; decreased levels may reflect altered lipid handling during acute MI. | |
| Arachidic acid | metabolite | 1 | — | — | Saturated long-chain fatty acid associated with increased atherogenic lipid metabolism and ACS risk. | |
| ARHGAP36ARHGAP36 | protein | 1 | — | ◆ | ARHGAP36 dysregulation contributes to vascular calcification and atherosclerotic plaque maturation in Type 1 MI. | |
| ATP-binding cassette transporter A5ABCA5 | protein | 1 | — | ◆ | ABC transporter regulating reverse cholesterol transport; altered expression modulates lipid burden in atherosclerotic lesions. | |
| Carbamylated LDL | lipid | 1 | — | — | Carbamylated LDL is an oxidatively modified lipoprotein variant retained in the subendothelium that triggers macrophage activation and plaque inflammation. | |
| Cartilage Intermediate Layer Protein 2CILP2 | protein | 1 | — | ◆ | CILP2 regulates oxidative lipid metabolism and lipoprotein handling in atherosclerotic plaque formation. | |
| Cer(d16:1/20:0) | lipid | 1 | — | — | Ceramide d16:1/20:0 accumulates in atherogenic conditions and modulates lipid metabolism and glucose-lipid coupling in atherosclerosis. | |
| Ceramide (18:0) | lipid | 1 | — | — | Ceramide (18:0) accumulates in atherosclerotic lesions and predicts adverse cardiovascular outcomes through altered lipid metabolism and plaque destabilization. | |
| Ceramide (24:0) | lipid | 1 | — | — | Ceramide (24:0) accumulates in atherosclerotic lesions and predicts adverse cardiovascular outcomes through altered lipid metabolism and plaque composition. | |
| Ceramide (24:1) | lipid | 1 | — | — | Ceramide (24:1) dysregulation predicts major adverse cardiovascular events through altered sphingolipid metabolism in atherosclerotic plaques. | |
| Ceramide C16:0 | lipid | 1 | — | — | Ceramide C16:0 accumulates in ischemic myocardium and drives cardiomyocyte apoptosis, predicting major adverse cardiovascular events. | |
| Ceramide d18:0/20:0 | lipid | 1 | — | — | A specific ceramide species enriched in calcified atherosclerotic plaque involved in lipid accumulation and vascular inflammation. | |
| Ceramide(d18:1/18:0) | lipid | 1 | — | — | Ceramide(d18:1/18:0) accumulation reflects lipid dysmetabolism and vascular inflammation in acute myocardial injury. | |
| Cholesterol ester | lipid | 1 | — | — | Cholesterol esters accumulate in atherosclerotic plaques and correlate with MI risk; elevated in vulnerable lesions. | |
| Chylomicron | lipoprotein | 1 | — | — | Chylomicron remnants are postprandial atherogenic lipoproteins that promote vascular inflammation and atherosclerotic plaque development. | |
| CO2CO2 | gene | 1 | — | — | CO2 mitochondrial dysfunction elevates ROS production, promoting oxidative lipid modification and systemic inflammation in obesity-associated CAD. | |
| DAZAP2DAZAP2 | gene | 1 | — | — | DAZAP2 is associated with atherosclerotic plaque progression, likely through effects on lipid metabolism or inflammatory-cell activation. | |
| Dehydrogenase/Reductase 13DHRS13 | gene | 1 | — | ◆ | DHRS13 dysregulation may alter lipid oxidation and atherogenic lipid accumulation. | |
| Diacyl-phosphatidylcholine C38:3 | lipid | 1 | — | — | Specific phosphatidylcholine species composition predicts plaque lipid burden and MI risk independent of standard lipid levels. | |
| Diacyl-phosphatidylcholine C40:4 | lipid | 1 | — | — | Specific phosphatidylcholine species composition predicts plaque lipid burden and MI risk independent of standard lipid levels. | |
| Diacylglycerol | lipid | 1 | — | — | Diacylglycerol accumulation drives lipotoxicity and contributes to atherosclerotic plaque lipid-core formation and lesion progression. | |
| Diacylglycerol (18:1/18:2) | lipid | 1 | — | — | Diacylglycerol species accumulate in atherosclerotic lesions and drive lipid-driven plaque inflammation and progression. | |
| Diacylglycerol 18:1_20:0 | lipid | 1 | — | — | Diacylglycerol 18:1_20:0 is a lipid biomarker of calcified coronary atherosclerotic plaque, reflecting advanced lesion mineralization. | |
| Diacylglycerol O-acyltransferase 2DGAT2 | gene | 1 | — | ◆ | DGAT2 regulates triacylglycerol formation affecting systemic and vascular lipid content. | |
| Dihexosylceramide d18:1/16:0 | lipid | 1 | — | — | A specific dihexosylceramide species enriched in calcified atherosclerotic plaque contributing to lipid retention. | |
| Dihydrosphingosine | lipid | 1 | — | — | Dihydrosphingosine elevation reflects altered sphingolipid metabolism associated with cardiovascular risk. | |
| Discs Large Homolog 2DLG2 | protein | 1 | — | ◆ | DLG2 represents a CAD-associated locus with pleiotropic roles in lipid metabolism and vascular signaling. | |
| DOCK7DOCK7 | gene | 1 | — | — | DOCK7 harbors ANGPTL3 regulatory variants affecting triglyceride-rich lipoprotein levels and plaque lipid burden. | |
| DystrophinDMD | protein | 1 | — | ◆ | DMD deficiency impairs vascular smooth-muscle integrity and lipid-handling capacity, contributing to atherosclerotic vulnerability. | |
| Endothelial lipaseLIPG | protein | 1 | — | ◆ | Endothelial lipase controls local lipid accumulation and endothelial lipoprotein metabolism in atherosclerosis. | |
| Enzymatically modified LDL | lipoprotein | 1 | — | — | An enzymatically modified LDL variant that enhances macrophage lipid uptake and promotes plaque inflammation and lipid retention. | |
| Ether glycerolipids | lipid | 1 | — | — | Ether glycerolipids in RBC membranes impair hemostasis and contribute to coronary atherosclerotic disease. | |
| Ether-phosphatidylcholine | lipid | 1 | — | — | Ether-phospholipids accumulate in atherosclerotic plaques and correlate with plaque progression and vulnerability. | |
| Ether-type phosphatidylethanolamines | lipid | 1 | — | — | Ether-type phosphatidylethanolamines are antioxidant lipids whose depletion reflects oxidative stress and advanced atherosclerotic disease. | |
| extremely large VLDL particles | lipoprotein | 1 | — | — | Extremely large VLDL particles are ApoB-containing lipoproteins that accumulate in the arterial intima, undergo oxidation, and initiate atherosclerotic plaque f | |
| F2-isoprostanes | metabolite | 1 | — | — | F2-isoprostanes are non-enzymatic lipid peroxidation products reflecting oxidative stress in atherosclerotic plaque and atherothrombotic progression. | |
| Fatty acyl esters of hydroxy fatty acids | lipid | 1 | — | — | Oxygenated lipid esters mark advanced lipid oxidation and plaque vulnerability. | |
| Free cholesterol | lipid | 1 | — | — | Free cholesterol accumulates in retained ApoB-lipoproteins and undergoes oxidation, initiating plaque formation and destabilization. | |
| Free fatty acids | lipid | 1 | — | — | Elevated free fatty acids promote lipid retention, oxidation, and plaque destabilization. | |
| Glycolithocholic acid | metabolite | 1 | — | — | A secondary bile acid whose reduction in male CAD associates with altered lipid metabolism and atherogenic dyslipidemia. | |
| Glycosylated HDL | lipoprotein | 1 | — | — | Glycosylated HDL is a dysfunctional HDL form that loses antiatherogenic properties and contributes to atherosclerosis risk. | |
| Glycosylated LDL | lipoprotein | 1 | — | — | Glycosylated LDL is a modified form retained in arterial intima and promotes atherogenesis through oxidative modification. | |
| GPI-anchored high-density lipoprotein-binding protein 1GPIHBP1 | protein | 1 | — | ◆ | GPIHBP1 anchors lipoprotein lipase at the endothelial surface, regulating triglyceride-rich lipoprotein clearance and lipid substrate retention. | |
| GSRGSR | gene | 1 | — | ◆ | GSR expression increases in response to oxidized-LDL, sustaining antioxidant capacity against oxidative modification of retained lipids. | |
| HDL Particle Number | lipoprotein | 1 | — | — | HDL particle number predicts cardiovascular event risk through reverse cholesterol transport efficiency. | |
| HDL-1 (large HDL) | lipoprotein | 1 | — | — | Large HDL particles mediate reverse cholesterol transport and protect against lipid retention and atherosclerosis progression. | |
| HDL3 | lipoprotein | 1 | — | — | HDL3 participates in reverse cholesterol transport with diminished antiplatelet capacity compared to HDL2. | |
| IgM anti-phosphorylcholine | protein | 1 | — | — | Reduced IgM anti-PC fails to neutralize oxidized phospholipid epitopes on atherogenic lipoproteins, increasing thrombotic risk. | |
| INSIG1INSIG1 | gene | 1 | — | ◆ | INSIG1 controls SREBP-mediated lipid synthesis, suppressing cholesterol uptake and regulating lipid accumulation in atherosclerotic plaques. | |
| Isoundecylic acid | metabolite | 1 | — | — | Branched-chain fatty acid associated with altered lipid metabolism and plaque vulnerability in atherosclerosis. | |
| KaptinKPTN | gene | 1 | — | ◆ | KPTN regulates lipid metabolism pathways contributing to CAD susceptibility. | |
| Kruppel Like Factor 14KLF14 | gene | 1 | — | — | KLF14 regulates lipid metabolism and ApoB-lipoprotein processing, modulating substrate for atherogenesis. | |
| LacCer(d18:1/16:0) | lipid | 1 | — | — | LacCer(d18:1/16:0) contributes to lipid retention and metabolic dysregulation in atherosclerotic lesions. | |
| LactoperoxidaseLPO | protein | 1 | — | ◆ | Lactoperoxidase-mediated oxidative stress contributes to lipoprotein oxidation and plaque destabilization. | |
| large VLDL particles | lipoprotein | 1 | — | — | Large VLDL particles are ApoB-containing lipoproteins that accumulate in the arterial intima, undergo oxidation, and initiate atherosclerotic plaque formation a | |
| LCATLCAT | protein | 1 | — | ◆ | LCAT controls phospholipid and cholesterol ester metabolism on HDL, influencing net atherogenic lipid burden. | |
| LDL-5 (small dense LDL) | lipoprotein | 1 | — | — | Small dense LDL particles are preferentially retained and oxidized in the arterial intima, driving early atherosclerotic lesion formation. | |
| LDL-sphingomyelins | lipid | 1 | — | — | LDL sphingomyelin content reflects lipoprotein composition changes; reduction by plant stanols lowers atherosclerotic burden. | |
| LDL-triacylglycerols | lipid | 1 | — | — | Elevated LDL triacylglycerol content indicates atherogenic lipoprotein remodeling that promotes intimal retention and oxidation. | |
| Lithocholic acid | metabolite | 1 | — | — | A secondary bile acid whose reduction in male CAD associates with altered lipid metabolism and atherogenic dyslipidemia. | |
| LPCAT3LPCAT3 | protein | 1 | — | ◆ | LPCAT3 catalyzes lipid peroxidation and oxidized-phospholipid remodeling, promoting oxidized-lipid accumulation in atherosclerotic plaques. | |
| Lysocardiolipin acyltransferase 1LCLAT1 | gene | 1 | — | ◆ | LCLAT1 remodels cardiolipin affecting mitochondrial function and ischemic vulnerability. | |
| Lysophosphatidylcholine (18:0) | lipid | 1 | — | — | Lysophosphatidylcholine is a lipid oxidation product and inflammatory mediator associated with lipoprotein modification and vascular inflammation in atheroscler | |
| Lysophosphatidylcholine O-18:1 | lipid | 1 | — | — | Lysophosphatidylcholine O-18:1 is a lipid signature of fibrotic noncalcified coronary plaque phenotype relevant to rupture vulnerability. | |
| Lysophosphatidylethanolamine (22:5/0:0) | lipid | 1 | — | — | Lysophosphatidylethanolamine is an oxidized phospholipid product that accumulates in atherosclerotic plaques and promotes inflammatory activation. | |
| Lysophosphatidylethanolamine 16:0 | lipid | 1 | — | — | Lysophosphatidylethanolamine 16:0 is enriched in lipid-rich noncalcified plaque, marking high-risk atherogenic lesions susceptible to rupture. | |
| Lysophosphatidylethanolamine 18:0 | lipid | 1 | — | — | Lysophosphatidylethanolamine 18:0 is enriched in lipid-rich noncalcified plaque, marking high-risk atherogenic lesions susceptible to rupture. | |
| Lysophosphatidylethanolamines | lipid | 1 | — | — | Elevated lysophosphatidylethanolamines reflect lipid remodeling and oxidative stress in atherosclerotic plaque. | |
| Lysophosphoethanolamines | lipid | 1 | — | — | Lysophosphoethanolamines accumulate in vulnerable plaques and promote lipid oxidation and inflammatory activation. | |
| Mannosyl (Alpha-1,3-)-Glycoprotein Beta-1,2-N-Acetylglucosaminyltransferase 1MGAT1 | protein | 1 | — | ◆ | MGAT1 influences glycosylation of lipoprotein and inflammatory mediators relevant to atherosclerosis. | |
| Matrix Gla proteinMGP | protein | 1 | — | ◆ | Under-carboxylated MGP reflects vitamin K2 insufficiency, permitting arterial calcification and atherosclerotic burden. | |
| Membrane bound O-acyltransferase domain-containing 2MBOAT2 | gene | 1 | — | ◆ | MBOAT2 regulates lipid remodeling in atherogenic lipoprotein metabolism and retention. | |
| Methylglyoxal | metabolite | 1 | — | — | Reactive dicarbonyl that generates advanced glycation end-products, accelerating lipid oxidation and plaque inflammation. | |
| microRNA-210MIR210 | rna | 1 | — | — | miR-210 suppresses lipid-oxidation pathways and promotes hypoxic responses, modulating plaque lipid metabolism and inflammation. | |
| microRNA-21aMIR21 | rna | 1 | — | — | miR-21a suppresses lipid-homeostasis genes and enhances inflammatory signaling in atherosclerotic plaque. | |
| microRNA-431-5pMIR431 | rna | 1 | — | — | miR-431-5p suppresses cholesterol and triglyceride metabolism genes, altering subendothelial lipid dynamics. | |
| microRNA-434-3pMIR434 | rna | 1 | — | — | miR-434-3p suppresses genes regulating lipoprotein metabolism, affecting subendothelial lipid accumulation. | |
| microRNA-677-5pMIR677 | rna | 1 | — | — | miR-677-5p suppresses cholesterol and triglyceride metabolism genes, altering subendothelial lipid dynamics. | |
| Minimally modified LDL | lipoprotein | 1 | — | — | Minimally modified LDL is a partially oxidized form that initiates endothelial dysfunction and early plaque inflammation. | |
| miR-10b-5p | rna | 1 | — | — | miR-10b-5p regulates cholesterol and LDL-C metabolism, affecting lipid substrate for atherogenesis. | |
| miR-1908-5p | rna | 1 | — | — | miR-1908-5p modulates lipid and glucose metabolism, influencing atherogenic lipoprotein burden. | |
| miR-199a | rna | 1 | — | — | miR-199a modulates lipid homeostasis and LDL-cholesterol levels, influencing atherothrombotic lipid burden. | |
| Monohexosylceramides | lipid | 1 | — | — | Monohexosylceramides are atherogenic lipid species that accumulate in plaques and promote inflammation. | |
| Monostearin | lipid | 1 | — | — | Monoglyceride lipid species reflecting lipid metabolism dysregulation in atherosclerotic lesion or post-intervention remodeling. | |
| Myristoylcarnitine | metabolite | 1 | — | — | Acylcarnitine accumulation reflects impaired mitochondrial fatty-acid oxidation and energy crisis in ischemic myocardium. | |
| Native LDL | lipoprotein | 1 | — | — | ApoB-lipoprotein subclass retained in subendothelial intima; substrate for oxidative modification initiating atherosclerosis. | |
| ND4ND4 | gene | 1 | — | — | ND4 variants that optimize mitochondrial function reduce ROS production, limiting oxidative lipid modification and plaque inflammation. | |
| ND5ND5 | gene | 1 | — | — | ND5 mitochondrial dysfunction elevates ROS production, amplifying lipid oxidation and plaque inflammation in atherosclerosis. | |
| OsteocalcinBGLAP | protein | 1 | — | ◆ | Carboxylated osteocalcin status reflects vitamin K2 sufficiency; deficiency increases atherosclerotic and ischemic risk. | |
| Oxidized Non-esterified Fatty Acids | metabolite | 1 | — | — | Oxidized non-esterified fatty acids promote oxidative stress and inflammation in atherosclerotic plaque development and destabilization. | |
| Oxidized phospholipid | lipid | 1 | — | — | Oxidized phospholipids associated with atherogenic lipoproteins promote inflammatory plaque remodeling and instability. | |
| Palmitelaidic acid | lipid | 1 | — | — | Trans-unsaturated fatty acid reflecting dyslipidemia and atherogenic lipid remodeling in acute coronary syndrome. | |
| Paraoxonase 2PON2 | protein | 1 | — | ◆ | Intracellular antioxidant enzyme limiting lipid peroxide formation and oxLDL generation during atherosclerotic lesion development. | |
| PDZ Domain Containing 1PDZK1 | gene | 1 | — | ◆ | PDZK1 scaffolding regulates SR-BI expression and HDL-mediated cholesterol efflux, influencing lipid retention in the subendothelium. | |
| Phosphatidylcholine 32:0 | lipid | 1 | — | — | Phosphatidylcholine 32:0 on LDL surface indicates aggregation-prone particle phenotype. | |
| Phosphatidylcholine 32:1 | lipid | 1 | — | — | Phosphatidylcholine 32:1 on LDL surface is associated with reduced aggregation propensity. | |
| Phosphatidylcholine aa C32:1 | lipid | 1 | — | — | Phosphatidylcholine species in lipoprotein particles; substrate for oxidative modification in atherosclerotic lesion formation. | |
| Phosphatidylcholine ae C32:2 | lipid | 1 | — | — | Ether-linked phosphatidylcholine species in lipoprotein particles; substrate for oxidative modification in atherosclerotic lesion. | |
| Phosphatidylcholines | lipid | 1 | — | — | Phosphatidylcholines serve as oxidizable substrates in atherogenic lipoproteins and plaque, generating pro-inflammatory oxidized species. | |
| Phosphatidylinositol 16:0/18:2 | lipid | 1 | — | — | Phosphatidylinositol species in LDL reflect lipid remodeling under statin therapy, indicating atherosclerotic lipid burden. | |
| Phosphatidylinositol 16:1/18:0 | lipid | 1 | — | — | Phosphatidylinositol species composition predicts lipid-lowering therapeutic efficacy. | |
| Phosphatidylinositol 18:0/18:1 | lipid | 1 | — | — | Phosphatidylinositol species reflect lipid composition changes in response to lipid-lowering therapy. | |
| Phosphatidylinositol 18:0/18:2 | lipid | 1 | — | — | Phosphatidylinositol species in LDL track lipid remodeling under therapeutic intervention. | |
| Phospholipase A2 Group IIEPLA2G2E | gene | 1 | — | ◆ | Secreted phospholipase regulating lipoprotein remodeling and lipid metabolism in atherosclerotic lesion formation. | |
| Phospholipid phosphatase-related protein 2PLPPR2 | gene | 1 | — | ◆ | PLPPR2 regulates phospholipid homeostasis affecting lipoprotein structure and atherogenicity. | |
| Phospholipid transfer proteinPLTP | protein | 1 | — | ◆ | PLTP facilitates lipoprotein remodeling and small dense LDL formation, promoting atherosclerotic plaque development. | |
| Plasmanyl phosphatidylcholine | lipid | 1 | — | — | Plasmanyl phosphatidylcholine is an antioxidant ether-lipid that reduces lipid peroxidation and atherosclerotic burden. | |
| Plasmenyl phosphatidylethanolamine | lipid | 1 | — | — | Plasmenyl phosphatidylethanolamine is an antioxidant ether-lipid that reduces lipid peroxidation and atherosclerotic burden. | |
| POVPC | lipid | 1 | — | — | An oxidized phosphatidylcholine species that accumulates in atherosclerotic plaques and triggers inflammatory macrophage activation. | |
| Protein carbonyl | metabolite | 1 | — | — | Oxidative stress marker reflecting protein oxidation in atherosclerotic plaque and lipid peroxidation. | |
| PTENPTEN | protein | 1 | — | ◆ | PTEN regulates phosphoinositide signaling and lipid metabolism, modulating vascular inflammation downstream of anti-inflammatory IL-37. | |
| QSER1QSER1 | gene | 1 | — | — | QSER1 is associated with lipid metabolism and atherogenic dyslipidemia in coronary disease. | |
| Regulator of G-protein signaling 19RGS19 | gene | 1 | — | ◆ | RGS19 influences APOB secretion and lipoprotein metabolism affecting CAD risk. | |
| Remnant lipoproteins | lipoprotein | 1 | — | — | Remnant lipoproteins accumulate in the subendothelial space and drive foam cell formation, initiating atherosclerotic plaque. | |
| SGPP2SGPP2 | gene | 1 | — | ◆ | SGPP2 regulates sphingosine-1-phosphate signaling, affecting lipid metabolism and plaque-cell activation during atherosclerotic progression. | |
| Sialidase | protein | 1 | — | — | Sialidase-mediated LDL desialylation increases lipoprotein retention and innate immune activation in the intima. | |
| SLCO1B1SLCO1B1 | gene | 1 | — | ◆ | SLCO1B1 encodes a transporter regulating LDL-cholesterol clearance and atherogenic lipoprotein levels. | |
| Sphingomyelin 36:3 | lipid | 1 | — | — | A specific sphingomyelin species enriched in calcified atherosclerotic plaque involved in lipoprotein structure and atherogenesis. | |
| Sphingomyelin 42:3;O2 | lipid | 1 | — | — | Sphingomyelin in LDL surface predicts particle aggregation and atherosclerotic lipid burden. | |
| Sphingomyelin Synthase 2SGMS2 | gene | 1 | — | ◆ | SGMS2 regulates ceramide and sphingomyelin metabolism, affecting lipoprotein atherogenicity and subendothelial lipid accumulation. | |
| Sphingomyelinase, AcidSMPD1 | gene | 1 | — | ◆ | SMPD1-catalyzed ceramide production from lipoprotein lipids drives endothelial activation and plaque inflammation. | |
| SREBF1SREBF1 | gene | 1 | — | ◆ | SREBF1 regulates lipid synthesis and inflammatory responses; its oxidative stress-linked dysregulation promotes lipid accumulation and atherosclerotic plaque fo | |
| StarD4STARD4 | protein | 1 | — | ◆ | StarD4 modulates intracellular cholesterol transport and availability, influencing lipid retention and atherosclerotic substrate dynamics. | |
| Sterol ester (27:1/18:2) | lipid | 1 | — | — | Sterol ester (27:1/18:2) is a causal metabolite in coronary atherosclerosis, enriched in atherosclerotic lipid cores and driving lesion progression. | |
| Superoxide Dismutase 3SOD3 | protein | 1 | — | ◆ | SOD3 scavenges superoxide to suppress LDL oxidation and inflammatory ROS production in plaques. | |
| Tetracosanoic acid | lipid | 1 | — | — | Very-long-chain fatty-acid accumulation reflects atherogenic lipid dysmetabolism and increased acute coronary-syndrome risk. | |
| Transmembrane and Tetratricopeptide Repeat Containing 2TMTC2 | protein | 1 | — | ◆ | TMTC2 modulates intracellular cholesterol trafficking and endothelial barrier integrity, influencing lipid retention and vascular dysfunction. | |
| Triacylglycerol (52:5) | lipid | 1 | — | — | Triacylglycerol (52:5) is a causal metabolite in coronary atherosclerosis, accumulated in atherogenic lipid cores and associated with lesion instability. | |
| Triacylglycerol (53:4) | lipid | 1 | — | — | Triacylglycerol species enriched in atherogenic lipoproteins promote plaque lipid accumulation and inflammation. | |
| Triacylglycerol 52:2 | lipid | 1 | — | — | Triacylglycerol 52:2 is a lipid biomarker of calcified coronary atherosclerotic plaque, reflecting mineral-associated lipid deposition. | |
| Triacylglycerol 52:3 | lipid | 1 | — | — | Triacylglycerol 52:3 is a lipid biomarker of calcified coronary atherosclerotic plaque, reflecting mineral-associated lipid deposition. | |
| Tribbles pseudokinase 1TRIB1 | gene | 1 | — | ◆ | TRIB1 modulates ApoC-III and ApoB-lipoprotein levels, regulating atherogenic lipid retention driving atherosclerotic plaque formation. | |
| Triglyceride-rich lipoproteins | lipoprotein | 1 | — | — | Triglyceride-rich lipoproteins contribute to lipid retention and oxidative modification in the subendothelium, driving atherosclerotic plaque initiation and gro | |
| Trihexosylceramides | lipid | 1 | — | — | Trihexosylceramides are atheroprotective lipid species whose reduction associates with proatherogenic lipidome composition. | |
| TXNTXN | gene | 1 | — | ◆ | TXN expression is induced by oxidized-LDL exposure and protects against lipid-driven oxidative stress in atherogenic lesions. | |
| TXNRD1TXNRD1 | gene | 1 | — | ◆ | TXNRD1 is induced by oxidative modification of retained lipids, mediating antioxidant defenses against atherogenic lipid burden. | |
| Vascular peroxidase 1VPO1 | protein | 1 | — | — | VPO1 catalyzes LDL oxidation in the subintimal space, triggering foam-cell formation and plaque inflammation. | |
| VLDL receptorVLDLR | protein | 1 | — | ◆ | VLDL receptor mediates atherogenic lipoprotein uptake and foam cell differentiation in atherosclerotic lesions. | |
| Zinc Finger E-Box Binding Homeobox 2ZEB2 | protein | 1 | — | ◆ | ZEB2 regulates lipid handling and vascular metabolic pathways, modulating atherosclerotic-plaque lipid retention and inflammation. | |
| 3-hydroxy-3-methylglutaryl-CoA reductaseHMGCR | gene | — | — | ✦◆ | HMGCR controls hepatic cholesterol synthesis; inhibition lowers LDL and reduces atherosclerotic plaque formation and MI risk. | |
| Bone Morphogenetic Protein 3BMP3 | gene | — | — | ✦◆ | BMP3 modulates osteogenic differentiation of vascular cells and lipid handling in plaque. | |
| Lipoprotein(a) Pseudogene 2LPAL2 | gene | — | — | ✦ | Genetic variant modulating lipoprotein(a) levels, a direct atherogenic risk factor. | |
| Myocyte enhancer factor 2AMEF2A | gene | — | — | ✦◆ | Controls vascular smooth muscle differentiation and anti-inflammatory gene expression in atherosclerosis. |
Plaque inflammation
Vascular inflammation473| Molecule | Type | Conf. | Refs | Trials | Evidence | Mechanism |
|---|---|---|---|---|---|---|
| C-reactive proteinCRP | protein | 60 | 8 | ✦◆ | hs-CRP is a systemic inflammatory marker reflecting plaque-driven inflammation and predicting atherothrombotic events. | |
| Interleukin-6IL6 | protein | 60 | 1 | ✦◆ | IL-6 promotes plaque inflammation and leukocyte recruitment, accelerating atherosclerotic instability and thrombotic risk. | |
| TNF-αTNF | protein | 60 | 1 | ✦◆ | TNF-α is a pro-inflammatory cytokine that promotes atherosclerotic plaque inflammation, macrophage recruitment, endothelial dysfunction, and oxidative stress dr | |
| Interleukin-1βIL1B | protein | 57 | — | ◆ | Interleukin-1β is a central inflammasome-derived cytokine that orchestrates atherosclerotic plaque inflammation, promotes endothelial dysfunction and procoagula | |
| MyeloperoxidaseMPO | protein | 40 | 1 | ✦◆ | Myeloperoxidase oxidizes LDL and generates reactive oxygen species in atherosclerotic plaques, promoting inflammation and endothelial dysfunction; also a marker | |
| Interleukin-10IL10 | protein | 28 | — | ◆ | Interleukin-10 is a protective anti-inflammatory cytokine that restrains atherosclerotic plaque inflammation and macrophage activation; its reduction by oxidize | |
| Lipoprotein-associated Phospholipase A2PLA2G7 | protein | 24 | 4 | ✦◆ | Lp-PLA2 generates inflammatory mediators from oxidized lipids within atherosclerotic plaques, promoting destabilization and rupture. | |
| Monocyte Chemoattractant Protein-1CCL2 | protein | 24 | — | ◆ | MCP-1 recruits monocytes to the atherosclerotic plaque and inflamed endothelium, sustaining plaque destabilization. | |
| Interleukin-18IL18 | protein | 21 | — | ◆ | Interleukin-18 is an inflammasome-processed cytokine that promotes atherosclerotic inflammation, immune activation, and plaque destabilization in the atherothro | |
| Interleukin-8CXCL8 | protein | 20 | — | ✦◆ | IL-8 is released during plaque inflammation and endothelial activation, recruiting neutrophils and amplifying platelet activation. | |
| AdiponectinADIPOQ | protein | 18 | — | ◆ | Adiponectin suppresses plaque inflammation and endothelial dysfunction, exerting cardioprotection against atherothrombotic injury. | |
| NLRP3 inflammasomeNLRP3 | protein | 15 | 1 | — | NLRP3 inflammasome activation in atherosclerotic plaques and post-MI inflammation generates IL-1β and IL-18, amplifying plaque destabilization and injury respon | |
| Interferon-GammaIFNG | protein | 14 | — | ◆ | IFN-γ amplifies macrophage activation and vascular inflammation in destabilized atherosclerotic plaques preceding Type 1 MI. | |
| Serum Amyloid ASAA1 | protein | 11 | — | ◆ | SAA is a major acute-phase protein elevated at plaque rupture, modifies HDL-mediated reverse cholesterol transport and amplifies vascular inflammation. | |
| CD40CD40 | gene | 10 | — | ◆ | CD40–CD40L interaction promotes endothelial activation, leukocyte recruitment, and platelet–leukocyte thromboinflammatory crosstalk. | |
| Interleukin-17AIL17A | protein | 10 | — | ✦◆ | IL-17A is a pro-inflammatory T-cell cytokine that destabilizes plaques, activates platelets, and promotes coronary thrombosis in Type 1 MI. | |
| Interleukin-2IL2 | protein | 10 | — | ◆ | IL-2 elevation promotes T-cell-mediated vascular inflammation and is associated with acute coronary syndrome. | |
| Pentraxin-3PTX3 | protein | 10 | — | ✦◆ | Pentraxin-3 mediates immune inflammation in atherosclerotic plaques and modulates platelet activation during thrombosis. | |
| S100A8S100A8 | protein | 10 | — | ◆ | S100A8 (calprotectin) drives sterile inflammation and thromboinflammation in acute MI, promoting infarct wall thinning and adverse remodeling. | |
| S100A9S100A9 | protein | 10 | — | ◆ | S100A9 (calprotectin) is a key alarmin amplifying vascular inflammation and thromboinflammation through monocyte recruitment and neutrophil-platelet interaction | |
| C-X-C Motif Chemokine Ligand 12CXCL12 | protein | 9 | — | ◆ | CXCL12 activates endothelial NF-κB signaling, recruits immune cells to atherosclerotic plaques, and mediates platelet–thrombosis interactions. | |
| CD14CD14 | protein | 9 | — | ✦◆ | CD14 marks monocyte and macrophage subsets that drive vascular inflammation, plaque destabilization, and contribute to platelet–leukocyte crosstalk during acute | |
| Toll-Like Receptor 4TLR4 | protein | 9 | — | ◆ | TLR4 promotes inflammasome signaling and oxidative stress in atherothrombotic plaque and platelets, driving MI progression. | |
| CDKN2BCDKN2B | gene | 8 | — | ✦ | CDKN2B variants affect vascular cell proliferation and inflammatory signaling, modulating atherosclerotic plaque development and rupture risk. | |
| OsteopontinSPP1 | protein | 8 | — | ✦◆ | Osteopontin promotes macrophage-fibroblast crosstalk and collagen remodeling, destabilizing the plaque and driving post-MI cardiac remodeling. | |
| Uric acid | metabolite | 8 | — | — | Uric acid accumulates during oxidative injury and endothelial dysfunction in acute MI, serving as a biomarker of inflammatory burden and CAD severity. | |
| calprotectin | protein | 7 | — | — | Neutrophil and macrophage-derived calcium-binding protein reflecting active plaque inflammation and thrombotic risk. | |
| Caspase-1CASP1 | protein | 7 | — | ◆ | Caspase-1 activates pro-inflammatory cytokines IL-1β and IL-18 via the NLRP3 inflammasome, promoting plaque inflammation and destabilization. | |
| Chitinase-3-Like Protein 1CHI3L1 | protein | 7 | — | ◆ | CHI3L1 reflects macrophage infiltration and inflammation within unstable plaques and drives matrix remodeling promoting rupture. | |
| HaptoglobinHP | protein | 7 | — | ◆ | Haptoglobin is an acute-phase diagnostic biomarker for myocardial infarction, responding to hemolysis and vascular inflammation in atherothrombotic events. | |
| VisfatinNAMPT | protein | 7 | — | ✦◆ | Visfatin amplifies plaque inflammation and matrix degradation, destabilizing atherosclerotic lesions and increasing rupture and thrombotic risk. | |
| Sirtuin 1SIRT1 | protein | 6 | 1 | ✦◆ | SIRT1 deacetylates NF-κB to suppress plaque inflammation and prothrombotic signaling, while preventing oxidized-LDL-induced endothelial dysfunction and cardiomy | |
| Cyclin-Dependent Kinase Inhibitor 2ACDKN2A | gene | 6 | — | ✦ | CDKN2A regulates cell-cycle arrest and senescence in vascular cells, modulating inflammatory responses and atherosclerotic plaque progression. | |
| Interleukin-1 Receptor AntagonistIL1RN | gene | 6 | — | ◆ | IL1RN suppresses IL-1-driven monocyte recruitment and pro-inflammatory cytokine amplification in atherosclerotic plaque. | |
| Interleukin-33IL33 | protein | 6 | — | ◆ | IL-33 mediates both pro-inflammatory responses in atherosclerotic plaques and stress-responsive cardioprotection during myocardial injury. | |
| MIF | protein | 6 | — | — | MIF drives atherosclerotic inflammation and thrombosis via macrophage recruitment and platelet activation in the acute coronary event. | |
| OsteoprotegerinTNFRSF11B | protein | 6 | — | ✦◆ | Osteoprotegerin regulates inflammation and calcification in atherosclerotic plaques, markers of plaque destabilization. | |
| Reactive oxygen species | metabolite | 6 | — | — | Reactive oxygen species generated during plaque inflammation oxidize lipids, activate platelets, and cause vascular dysfunction in Type 1 MI. | |
| Soluble urokinase plasminogen activator receptorPLAUR | protein | 6 | — | ◆ | suPAR amplifies leukocyte recruitment and vascular inflammation, exacerbating plaque destabilization and coronary thrombosis. | |
| Bilirubin | metabolite | 5 | 1 | — | Bilirubin exerts antioxidant and antithrombotic effects, with low levels predicting thrombus burden and adverse outcomes in Type 1 MI. | |
| CXCL10CXCL10 | protein | 5 | — | ◆ | CXCL10 recruits T cells and monocytes to atherosclerotic lesions, amplifying plaque inflammation. | |
| IL-6 ReceptorIL6R | gene | 5 | — | ✦◆ | IL-6 receptor mediates IL-6 pro-inflammatory and myocardial-injury signaling in atherosclerosis and acute MI. | |
| Interleukin-4IL4 | protein | 5 | — | ◆ | IL-4 shifts macrophage polarization toward repair phenotype and is dysregulated in ACS, influencing post-MI injury and remodeling. | |
| Placental growth factorPGF | protein | 5 | — | ◆ | Placental growth factor drives angiogenesis and plaque inflammation; elevated levels independently predict ischemic events and plaque instability. | |
| Platelet-derived growth factor | protein | 5 | — | — | PDGF released from activated platelets promotes plaque inflammation and fibrous-cap vulnerability. | |
| Secretory phospholipase A2 | protein | 5 | — | — | Inflammatory phospholipase hydrolyzing lipoprotein phospholipids, generating pro-atherogenic lipid mediators. | |
| Aldosterone | metabolite | 4 | 1 | — | Aldosterone promotes vascular inflammation, endothelial dysfunction, and atherosclerotic plaque progression through mineralocorticoid-receptor signaling. | |
| C-C chemokine receptor type 2CCR2 | protein | 4 | 1 | ◆ | CCR2 mediates monocyte chemotaxis and adhesion into the atherosclerotic plaque, driving plaque inflammation and destabilization. | |
| Lipopolysaccharide | metabolite | 4 | 1 | — | Lipoprotein-transported endotoxin triggers TLR-mediated plaque inflammation and atherosclerosis progression. | |
| ANRIL | rna | 4 | — | — | ANRIL lncRNA at the 9p21.3 CAD locus regulates epigenetic pathways driving atherosclerotic inflammation and vascular disease. | |
| CD18ITGB2 | protein | 4 | — | ◆ | CD18 (β2-integrin) mediates monocyte and neutrophil adhesion and activation in plaque inflammation and reperfusion injury. | |
| CD44CD44 | gene | 4 | — | ◆ | CD44 mediates leukocyte-endothelial interactions, macrophage infiltration, and cell death pathways in atherosclerotic plaque inflammation and erosion. | |
| CDKN2B-AS1CDKN2B-AS1 | rna | 4 | — | ✦ | CDKN2B-AS1 is a 9p21 locus CAD-risk lncRNA that epigenetically controls smooth-muscle-cell function and atherosclerotic inflammation. | |
| FES Proto-Oncogene, Tyrosine KinaseFES | gene | 4 | — | ✦◆ | Tyrosine kinase modulating vascular smooth-muscle and endothelial inflammation; CAD and hypertension risk via arterial remodeling. | |
| Ficolin-2FCN2 | protein | 4 | — | ◆ | Ficolin-2 recognizes danger-associated patterns, activating complement and promoting plaque inflammation during acute MI. | |
| GelsolinGSN | protein | 4 | — | ◆ | Actin-modulating protein with anti-inflammatory and vascular-protective roles; downregulated in acute coronary inflammation. | |
| Glutathione peroxidase 4GPX4 | protein | 4 | — | ◆ | GPX4 suppresses ferroptotic cell death and lipid peroxidation in atherosclerotic lesions and post-ischemic myocardium. | |
| Inducible Nitric Oxide SynthaseNOS2 | gene | 4 | — | ✦◆ | iNOS-driven nitric oxide production in macrophages sustains plaque inflammation and impairs endothelial function. | |
| Interleukin-12IL12A | protein | 4 | — | ◆ | IL-12 drives Th1-mediated immune response and predicts major adverse cardiovascular events in acute coronary syndrome. | |
| Leucine-rich alpha-2-glycoprotein 1LRG1 | protein | 4 | — | ◆ | LRG1 is an inflammation-responsive acute-phase marker upregulated during plaque inflammation and myocardial ischemia in Type 1 MI. | |
| Leukotriene B4 | metabolite | 4 | — | — | Leukotriene eicosanoid recruiting leukocytes and amplifying vascular inflammation after MI. | |
| Lysophospholipids | lipid | 4 | — | — | Lysophospholipids are potent inflammatory mediators generated by phospholipase A2 that recruit leukocytes, activate platelets, and destabilize plaques. | |
| miR-21-5p | rna | 4 | — | — | miR-21-5p is an acute MI biomarker that regulates antioxidant responses (SOD2) and vascular inflammation. | |
| Peptidoglycan recognition protein 1PGLYRP1 | protein | 4 | — | ◆ | PGLYRP1 acts as a pattern recognition receptor promoting innate immune activation and plaque inflammation, with increased levels marking thrombotic burden in ST | |
| Scavenger Receptor A1MSR1 | protein | 4 | — | ◆ | Macrophage scavenger receptor recognizing oxidized and modified lipoproteins, driving foam cell formation and plaque inflammation. | |
| Signal Transducer and Activator of Transcription 3STAT3 | protein | 4 | — | ◆ | STAT3 activation by IL-10 restrains macrophage-driven plaque inflammation and vascular endothelial activation, reducing atherosclerotic destabilization. | |
| TNF Receptor Superfamily 1BTNFRSF1B | protein | 4 | — | ◆ | TNF receptor 2 regulates vascular inflammation and immune cell activation within atherosclerotic lesions. | |
| Toll-like receptor 2TLR2 | protein | 4 | — | ◆ | TLR2 activation by damage-associated or pathogen-associated molecular patterns in plaque drives inflammation and platelet recruitment. | |
| 5-LipoxygenaseALOX5 | protein | 3 | 2 | ◆ | 5-Lipoxygenase produces leukotrienes that regulate inflammatory cell recruitment and resolution post-MI. | |
| Acyl-CoA Synthetase Long Chain Family Member 4ACSL4 | protein | 3 | — | ◆ | Acyl-CoA synthetase that activates polyunsaturated fatty acids for ferroptotic lipid peroxidation, a mechanism linking macrophage oxidative stress to plaque inf | |
| Annexin A1ANXA1 | protein | 3 | — | ◆ | Annexin A1 downregulation after plaque rupture indicates disruption of local anti-inflammatory signaling and heightened plaque destabilization. | |
| C-X-C chemokine receptor type 3CXCR3 | protein | 3 | — | ◆ | CXCR3 transduces chemokine signals recruiting inflammatory Th1 cells and monocytes to destabilize plaques. | |
| C-X-C Motif Chemokine Ligand 1CXCL1 | protein | 3 | — | ◆ | CXCL1 recruits leukocytes to the atherosclerotic plaque, amplifying vascular inflammation and destabilization. | |
| C-X-C motif chemokine ligand 2CXCL2 | gene | 3 | — | ◆ | CXCL2 recruits leukocytes and promotes smooth muscle remodeling in vulnerable plaques. | |
| C-X-C motif chemokine receptor 7CXCR7 | protein | 3 | — | — | CXCR7 coordinates chemotaxis and platelet-leukocyte interactions during plaque inflammation and early thrombotic response in Type 1 MI. | |
| CD163CD163 | protein | 3 | — | ◆ | CD163 marks macrophage activation and plaque progression in atherosclerosis; functions as hemoglobin-haptoglobin receptor in vascular inflammation and MI pathog | |
| CD68CD68 | protein | 3 | — | ◆ | Macrophage surface antigen marking monocyte/macrophage accumulation that destabilizes atherosclerotic plaque and signals rupture vulnerability. | |
| CDCP1CDCP1 | protein | 3 | — | ◆ | CDCP1 mediates leukocyte adhesion, vascular inflammation and fibrosis in atherosclerotic plaque instability. | |
| ChemerinCMKLR1 | protein | 3 | — | ◆ | Chemerin recruits innate immune cells and activates macrophages, driving plaque inflammation and destabilization in acute coronary syndromes. | |
| Complement component C5C5 | protein | 3 | — | ◆ | Complement-pathway effector generating C5a to recruit leukocytes and amplify thromboinflammatory response in acute coronary syndrome. | |
| Cysteine-rich angiogenic inducer 61CYR61 | protein | 3 | — | — | CYR61 drives vascular inflammation and plaque vulnerability in acute coronary syndromes, predicting adverse outcomes. | |
| Electronegative LDL (L5) | lipoprotein | 3 | — | — | Electronegative LDL (L5) is a highly oxidized lipoprotein subspecies that triggers monocyte recruitment and macrophage activation, amplifying plaque inflammatio | |
| Fractalkine (CX3CL1)CX3CL1 | protein | 3 | — | ✦◆ | Monocyte-adhesion molecule and platelet–leukocyte crosstalk mediator in plaque inflammation and atherothrombotic thrombus formation. | |
| FurinFURIN | gene | 3 | — | ✦◆ | FURIN processes precursors of inflammatory cytokines and proteases that destabilize atherosclerotic plaques and promote endothelial dysfunction. | |
| Gasdermin DGSDMD | protein | 3 | — | ◆ | Gasdermin D mediates pyroptotic cardiomyocyte death and inflammatory cytokine release during acute myocardial infarction. | |
| GlycA | metabolite | 3 | — | — | GlycA is a glycoprotein-bound inflammation marker that correlates with monocyte recruitment and plaque destabilization in Type 1 MI pathogenesis. | |
| Heat-shock protein 60HSPD1 | protein | 3 | — | ◆ | Heat-shock protein 60 released from damaged mitochondria acts as a pathogen-associated molecular pattern to initiate and sustain atherosclerotic inflammation. | |
| High-mobility group box 1HMGB1 | protein | 3 | — | ◆ | High-mobility group box 1 (HMGB1) is a damage-associated molecular pattern released during ischemic injury that amplifies vascular inflammation and platelet thr | |
| Histone Deacetylase 9HDAC9 | gene | 3 | — | ◆ | HDAC9 genetic variants regulate histone acetylation and chromatin remodeling to modulate atherosclerotic plaque inflammation and stability. | |
| HLA-CHLA-C | gene | 3 | — | ◆ | HLA-C regulates immune recognition and endothelial activation; downregulation in AMI compromises inflammatory control and plaque stabilization. | |
| Immunoglobulin A | protein | 3 | — | — | IgA levels reflect adaptive immune activation in plaque inflammation and are altered post-MI. | |
| Integrin Alpha-L (CD11a)ITGAL | protein | 3 | — | ◆ | ITGAL mediates monocyte and T-cell recruitment into atherosclerotic plaques and crosstalk with platelet surfaces, amplifying plaque inflammation. | |
| Interleukin-17EIL17F | protein | 3 | — | ◆ | IL-17E drives vascular inflammation and predicts post-MI cardiac remodeling through pro-inflammatory T-cell signaling. | |
| Interleukin-6 signal transducerIL6ST | protein | 3 | — | ◆ | gp130 transduces IL-6 trans-signaling, amplifying monocyte recruitment and atherosclerotic inflammation. | |
| Jun proto-oncogene, AP-1 transcription factor subunitJUN | gene | 3 | — | ◆ | JUN orchestrates inflammatory gene programs destabilizing atherosclerotic plaques. | |
| L-selectinSELL | protein | 3 | — | ◆ | L-selectin on monocytes and neutrophils binds endothelial ligands, mediating leukocyte rolling, tethering and recruitment into inflamed atherosclerotic plaques. | |
| lactosylceramide | lipid | 3 | — | — | Lactosylceramide regulates monocyte recruitment and inflammatory signaling, bridging lipid retention and plaque inflammation. | |
| M-CSFCSF1 | protein | 3 | — | ◆ | M-CSF (CSF1) is a macrophage growth factor that recruits and activates monocytes, amplifying plaque inflammation in Type 1 MI and post-MI complications. | |
| MIAT (myocardial-infarction-associated transcript)MIAT | rna | 3 | — | — | Long non-coding RNA dysregulated in atherosclerosis and myocardial infarction, modulating vascular inflammation and plaque stability. | |
| Mitochondrial DNA (mtDNA) | other | 3 | — | — | mtDNA released from injured cells activates pattern-recognition receptors to trigger innate immune activation and plaque inflammation in atherosclerosis. | |
| Myeloperoxidase-oxidized LDL | lipoprotein | 3 | — | — | Myeloperoxidase-oxidized LDL is an inflammatory lipoprotein modification that promotes foam cell differentiation and endothelial dysfunction. | |
| Neopterin | metabolite | 3 | — | — | Neopterin is released by activated macrophages and monocytes, serving as a marker of immune activation and inflammation within destabilized atherosclerotic plaq | |
| Neutrophil elastaseELA2 | protein | 3 | — | — | Neutrophil elastase is released by activated neutrophils during NETosis and serves as a marker of neutrophil extracellular trap (NET)-driven immunothrombotic in | |
| Nuclear factor kappa B subunit 1NFKB1 | gene | 3 | — | ◆ | NFKB1 drives inflammatory gene expression in atherosclerosis and post-MI immune activation. | |
| Platelet-Derived Growth Factor DPDGFD | gene | 3 | — | ◆ | PDGFD promotes smooth-muscle-cell recruitment and phenotypic switching that destabilize the atherosclerotic plaque. | |
| RANTESCCL5 | protein | 3 | — | ◆ | RANTES (CCL5) recruits monocytes and macrophages to inflamed atherosclerotic plaques and directly activates platelets, amplifying vascular inflammation. | |
| Retinol-Binding Protein 4RBP4 | protein | 3 | — | ◆ | RBP4 is an adipokine associated with vascular inflammation and ischemic event risk, linking epicardial adipose-tissue remodeling to atherothrombotic progression | |
| S100A12S100A12 | protein | 3 | — | ◆ | S100A12 is a core plaque-rupture and vascular inflammation marker shared across atherothrombotic events; modulates MMP activity and immune activation in MI path | |
| Serpin Family A Member 3SERPINA3 | gene | 3 | — | ◆ | SERPINA3 is an acute-phase inflammatory marker upregulated in atherosclerotic plaques and predicts outcomes in myocardial infarction. | |
| SMAD3SMAD3 | gene | 3 | — | ✦◆ | SMAD3 is a CAD-risk effector in smooth muscle cells that controls TGF-β-mediated inflammation, matrix remodeling, and fibrous-cap stability. | |
| SMARCA4SMARCA4 | gene | 3 | — | ✦◆ | SMARCA4 influences DNA methylation and vascular smooth-muscle-cell behavior, modulating oxidative stress-linked pathways in MI susceptibility. | |
| Superoxide dismutase | protein | 3 | — | — | SOD catalyzes superoxide dismutation; reduced activity or expression reflects failed antioxidant defense in atherosclerotic inflammation and endothelial injury. | |
| lipoxygenase | protein | 2 | 2 | — | Lipoxygenase catalyzes arachidonic acid oxidation to pro-inflammatory and pro-thrombotic lipid mediators in plaque inflammation. | |
| ResistinRETN | protein | 2 | 1 | ◆ | Resistin promotes atherosclerotic inflammation and lipid dysregulation, increasing Type 1 MI recurrence risk. | |
| 12(S)-HETE | lipid | 2 | — | — | Proinflammatory eicosanoid mediating leukocyte recruitment and vascular inflammation post-MI. | |
| 20-HETE | metabolite | 2 | — | — | Eicosanoid metabolite driving adverse cardiovascular effects and plaque inflammation post-PCI. | |
| Adrenergic Receptor Beta-2ADRB2 | gene | 2 | — | ✦◆ | ADRB2-mediated signaling modulates neutrophil infiltration and inflammatory cell crosstalk in myocardial injury. | |
| Agouti-related peptideAGRP | gene | 2 | — | ◆ | Inflammatory peptide implicated in insulin signaling–atherosclerosis crosstalk and acute-phase response in MI. | |
| Arginase-1ARG1 | gene | 2 | — | ◆ | ARG1 marks alternatively-activated macrophages that modulate inflammatory responses and plaque stability during acute coronary syndrome. | |
| BCAR1BCAR1 | gene | 2 | — | ◆ | BCAR1 regulates vascular smooth muscle cell adhesion and endothelial function in atherosclerotic plaque development. | |
| C-C Motif Chemokine Ligand 23CCL23 | protein | 2 | — | ◆ | CCL23 recruits monocytes to sites of plaque inflammation and modulates fibrinolytic responses following thrombus formation. | |
| C-X-C motif chemokine ligand 13CXCL13 | protein | 2 | — | ◆ | CXCL13 recruits B cells and reprograms macrophages into pro-thrombotic niches, intensifying plaque inflammation. | |
| C–C Motif Chemokine Ligand 17CCL17 | protein | 2 | — | ◆ | CCL17 mediates post-MI plaque inflammation while also representing a cardioprotective anti-inflammatory signaling axis downstream of SGLT2-inhibitor treatment. | |
| Calbindin-2CALB2 | protein | 2 | — | — | CALB2 is enriched in advanced atherosclerotic plaques and associates with plaque inflammation and destabilization in Type 1 MI. | |
| cAMP Responsive Element ModulatorCREM | protein | 2 | — | — | CREM regulates T cell inflammatory responses post-MI, contributing to plaque destabilization and inflammation. | |
| Catechol-O-methyltransferaseCOMT | protein | 2 | — | ◆ | COMT regulates catecholamine and estrogen metabolism, influencing vascular inflammation and thrombotic risk in coronary artery disease. | |
| CCAAT/enhancer binding protein alphaCEBPA | gene | 2 | — | — | CEBPA regulates macrophage polarization and lipid handling in plaque inflammation. | |
| CCL22CCL22 | protein | 2 | — | ◆ | CCL22 chemokine recruits monocytes and regulates M2 macrophage polarization in atherosclerotic plaque inflammation. | |
| CD16FCGR3A | protein | 2 | — | ◆ | CD16 identifies pro-inflammatory monocyte subsets that are enriched in acute coronary syndromes and drive vascular inflammation and platelet activation during a | |
| citrullinated histone H3H3C1 | protein | 2 | — | — | NETosis product serving as specific marker of neutrophil extracellular trap burden and pathogenic plaque inflammation. | |
| Complement C1s serine proteaseC1S | gene | 2 | — | ◆ | C1S genetic variants amplify complement-driven vascular inflammation increasing atherosclerotic instability risk. | |
| Complement C5b-9 (MAC) | complex | 2 | — | — | C5b-9 amplifies endothelial injury and inflammatory cell recruitment through complement-driven lysis and activation. | |
| Complement factor HCFH | protein | 2 | — | ◆ | Complement regulator affecting inflammatory burden and post-MI ventricular remodeling, predicting long-term cardiovascular outcomes. | |
| Connective Tissue Growth FactorCTGF | protein | 2 | — | — | CTGF drives cardiac fibrosis and plaque inflammation through JCAD-dependent pro-atherogenic signaling in Type 1 MI. | |
| Cytochrome b-245 Alpha SubunitCYBA | gene | 2 | — | ◆ | CYBA is the core component of NADPH oxidase driving oxidative stress in plaque inflammation and lipid oxidation. | |
| Fetuin-AAHSG | protein | 2 | — | ✦◆ | Fetuin-A suppresses inflammatory and calcification processes in atherosclerotic plaque and contributes to post-MI cardiac dysfunction. | |
| Galectin-2LGALS2 | protein | 2 | — | ◆ | LGALS2 is a susceptibility locus for myocardial infarction, potentially mediating immune-inflammatory mechanisms in plaque biology. | |
| Granzyme AGZMA | gene | 2 | — | ◆ | Serine protease from activated lymphocytes contributing to plaque inflammation and fibrous-cap degradation. | |
| HemopexinHPX | protein | 2 | — | ◆ | Hemopexin mitigates heme-mediated oxidative injury and inflammation during atherothrombotic plaque destabilization and myocardial ischemia. | |
| HLA-DQB1HLA-DQB1 | gene | 2 | — | — | HLA-DQB1 is a CAD susceptibility locus that influences inflammatory pathway activation in coronary atherothrombosis. | |
| IL2RBIL2RB | gene | 2 | — | ◆ | IL2RB modulates adaptive immune responses and inflammatory cell recruitment contributing to atherosclerotic plaque destabilization. | |
| Indoleamine 2,3-dioxygenase 1IDO1 | protein | 2 | — | ◆ | IDO1 drives tryptophan catabolism to kynurenine in thrombi macrophages, amplifying plaque inflammation and destabilization. | |
| Insulin-like Growth Factor Binding Protein 6IGFBP6 | protein | 2 | — | ◆ | IGFBP6 regulates insulin-like growth factor availability during plaque inflammation and fibrous-cap degradation. | |
| Interleukin-35IL35 | protein | 2 | — | — | IL-35 exerts anti-inflammatory suppression within atherosclerotic plaques, protecting against destabilization and thrombosis. | |
| Interleukin-37IL37 | protein | 2 | — | ◆ | IL-37 exerts broad anti-inflammatory effects that dampen atherosclerotic plaque inflammation and protect against ischemic injury. | |
| Interleukin-5IL5 | gene | 2 | — | ◆ | Eosinophil-recruiting cytokine implicated in atherogenic immune response and plaque inflammation. | |
| IRAK3IRAK3 | gene | 2 | — | ◆ | IRAK3 negatively regulates TLR-driven inflammatory signaling, controlling monocyte activation and plaque inflammation in acute coronary events. | |
| Macrophage Migration Inhibitory Factor-2D-DT | protein | 2 | — | — | MIF-2 promotes plaque inflammation and atherosclerosis via chemokine and lipogenic signaling. | |
| Metastasis-associated lung adenocarcinoma transcript 1MALAT1 | rna | 2 | — | — | MALAT1 regulates inflammatory immune-cell recruitment and atherosclerotic plaque development. | |
| Milk Fat Globule-EGF Factor 8MFGE8 | gene | 2 | — | ◆ | MFGE8 participates in atherosclerotic plaque inflammation and may exert cardioprotective effects during myocardial stress. | |
| MIP-1αCCL3 | protein | 2 | — | ◆ | MIP-1α (CCL3) is a macrophage-derived chemokine that recruits monocytes and leukocytes, amplifying plaque inflammation and post-MI complications. | |
| MIP-3αCCL20 | protein | 2 | — | ◆ | MIP-3α (CCL20) is a chemokine that recruits lymphocytes and monocytes, contributing to post-MI inflammation and adverse remodeling. | |
| miR-15a-5p | rna | 2 | — | — | miR-15a-5p serves as a STEMI diagnostic biomarker with regulatory roles in endothelial cell inflammation. | |
| miR-221-3p | rna | 2 | — | — | miRNA marking inflammatory activation and vascular instability in unstable coronary lesions. | |
| miR-222-3p | rna | 2 | — | — | miR-222-3p directly suppresses SOD2 and regulates vascular performance in MI and heart failure. | |
| Monocyte Chemoattractant Protein-3CCL7 | protein | 2 | — | ◆ | MCP-3 recruits monocytes into the atherosclerotic plaque, amplifying vascular inflammation and plaque destabilization. | |
| MPO-DNA | other | 2 | — | — | Circulating NET component serving as marker of pathogenic neutrophil activation and thrombo-inflammatory burden post-MI. | |
| PAD4PADI4 | protein | 2 | — | ◆ | Enzyme mediating neutrophil extracellular trap formation, amplifying plaque inflammation and thrombotic burden. | |
| RANKTNFRSF11A | protein | 2 | — | ◆ | RANK (TNF receptor superfamily 11A) regulates inflammatory pathways and is associated with long-term MI mortality risk. | |
| RANKL (TNF Ligand Superfamily Member 11)TNFSF11 | protein | 2 | — | ◆ | RANKL modulates immune-cell activation and osteoclastogenesis; decreased levels in MI may reflect altered inflammatory and vascular-remodeling pathways. | |
| Selenoprotein SSELENOS | gene | 2 | — | ◆ | SELENOS encodes a redox-active selenoprotein that modulates oxidative stress and endoplasmic-reticulum inflammation, reducing atherosclerosis progression. | |
| Serine Protease Inhibitor A5SERPINA5 | protein | 2 | — | ◆ | SERPINA5 upregulation in CAD reflects heightened proteolytic and inflammatory activity destabilizing plaques. | |
| Signal Transducer and Activator of Transcription 1STAT1 | gene | 2 | — | ◆ | A transcription factor regulating inflammatory and injury responses in acute MI, modulating plaque inflammation and cardiomyocyte damage. | |
| Sirtuin 3SIRT3 | protein | 2 | — | ◆ | SIRT3 modulates macrophage oxidative stress and inflammation, with reduced activity contributing to plaque destabilization and Type 1 MI risk. | |
| Solute Carrier Family 7 Member 11SLC7A11 | protein | 2 | — | ◆ | System xc- antiporter that suppresses ferroptosis-driven lipid peroxidation and inflammatory cell death in atherosclerotic plaque macrophages. | |
| Spondin 1SPON1 | protein | 2 | — | ◆ | SPON1 modulates inflammation and vascular remodeling in spontaneous coronary dissection. | |
| T-cell Immunoglobulin and Mucin-domain containing-1TIMD4 | protein | 2 | — | ◆ | TIM-1 modulates immune tolerance and inflammatory responses in acute coronary syndrome pathogenesis. | |
| Vascular Non-Inflammatory Molecule 3 (Pantetheinase VNN3)VNN3 | gene | 2 | — | — | VNN3 upregulation amplifies oxidative stress and endothelial inflammation in acute MI. | |
| 15-epi-lipoxin A4 | metabolite | 1 | 1 | — | 15-epi-lipoxin A4 is an aspirin-triggered anti-inflammatory lipid mediator that limits plaque inflammation and platelet recruitment. | |
| Leukotriene | metabolite | 1 | 1 | — | Leukotrienes are arachidonic-acid-derived eicosanoids that potently recruit and activate leukocytes, amplifying plaque inflammation and the thrombotic response. | |
| 11-HDoHE | metabolite | 1 | — | — | 11-HDoHE reduces pro-thrombotic and pro-inflammatory signaling, protecting against atherothrombotic occlusion. | |
| 12-HEPE | metabolite | 1 | — | — | 12-HEPE attenuates post-MI inflammation and promotes resolution of plaque inflammation through lipid mediator signaling. | |
| 12,13-dihydroxy-octadecenoic acid | metabolite | 1 | — | — | 12,13-diHOME is an oxidized polyunsaturated fatty acid metabolite reflecting systemic lipid peroxidation and vascular inflammation in acute coronary syndromes. | |
| 12(S)-HPETE | lipid | 1 | — | — | Lipoxygenase metabolite amplifying inflammation and oxidative stress in acute myocardial infarction. | |
| 15-oxo-ETE | metabolite | 1 | — | — | 15-oxo-ETE is a pro-inflammatory lipid metabolite that drives monocyte recruitment and endothelial activation during plaque inflammation. | |
| 16-HETE | metabolite | 1 | — | — | Oxylipin lipid mediator promoting vascular inflammation and thrombotic event susceptibility. | |
| 16,17-EDP | metabolite | 1 | — | — | 16,17-EDP, derived from omega-3 PUFA, restrains platelet activation and leukocyte recruitment. | |
| 20-HDoHE | metabolite | 1 | — | — | 20-HDoHE suppresses platelet aggregation and inflammatory cell recruitment, limiting thrombus expansion. | |
| 3-Hydroxyfatty acid | metabolite | 1 | — | — | 3-Hydroxyfatty acid from LPS-containing lipoproteins activates innate immune sensors and plaque inflammation. | |
| 3-nitrotyrosine | metabolite | 1 | — | — | 3-nitrotyrosine accumulation reflects reactive nitrogen species generation by activated leukocytes and platelets during thrombotic coronary occlusion. | |
| 3-OMD | metabolite | 1 | — | — | 3-OMD is a tryptophan metabolite elevated in plaque-rupture phenotype, marking inflammatory destabilization and MACE risk. | |
| 8-hydroxy-2'-deoxyguanosine | metabolite | 1 | — | — | 8-OHdGuo reflects oxidative DNA damage in inflammatory cells and endothelium during atherosclerotic plaque inflammation and endothelial dysfunction. | |
| 8-isoprostane | metabolite | 1 | — | — | 8-isoprostane is a stable F2-isoprostane generated by oxidative modification of arachidonic acid in inflamed plaque and dysfunctional endothelium. | |
| 8,9-DiHETrE | metabolite | 1 | — | — | Oxylipin inflammatory mediator associated with plaque inflammation and cardiovascular thrombotic events. | |
| AC004485.3 | rna | 1 | — | — | AC004485.3 circulating levels reflect macrophage apoptosis and autophagy dysregulation in destabilizing atherosclerotic plaques. | |
| AC004920.3 | rna | 1 | — | — | AC004920.3 circulating levels reflect macrophage apoptosis and autophagy dysregulation in destabilizing atherosclerotic plaques. | |
| Acetyl-CoA carboxylase 1ACACA | protein | 1 | — | ◆ | ACC1 catalyzes malonyl-CoA synthesis, promoting fatty acid and inflammatory lipid production in plaque macrophages. | |
| Acidic mammalian chitinaseCHIA | protein | 1 | — | ◆ | Chitinase enzyme reflecting innate immune activation and inflammatory burden during acute MI, predicting post-MI remodeling. | |
| ACSP75 | peptide | 1 | — | — | ACSP75 is a urinary peptide biomarker that predicts acute coronary syndrome risk, potentially reflecting systemic or local vascular inflammation. | |
| Activin AINHBA | gene | 1 | — | ◆ | Activin A exerts anti-inflammatory and cardioprotective effects in acute coronary syndrome, limiting plaque inflammation and myocardial injury. | |
| Adenosine KinaseADK | protein | 1 | — | ◆ | ADK modulates adenosine-mediated inflammatory and metabolic signaling in atherosclerosis. | |
| ADTRPADTRP | gene | 1 | — | ◆ | ADTRP promotes sex-hormone-mediated suppression of monocyte recruitment and vascular inflammation, reducing plaque destabilization. | |
| AIM2AIM2 | protein | 1 | — | — | AIM2 inflammasome activation promotes plaque inflammation and destabilization in atherosclerotic disease and acute coronary events. | |
| AJ006998.2 | rna | 1 | — | — | AJ006998.2 circulating levels reflect macrophage apoptosis and autophagy dysregulation in destabilizing atherosclerotic plaques. | |
| ALCAMALCAM | protein | 1 | — | ◆ | ALCAM on circulating vesicles enhances leukocyte–endothelial adhesion and platelet–leukocyte coupling in acute MI. | |
| ALKBH1ALKBH1 | gene | 1 | — | ◆ | ALKBH1-mediated m6A demethylation regulates inflammatory cytokine and matrix-metalloproteinase expression, influencing plaque inflammation and fibrous-cap stabi | |
| Allograft Inflammatory Factor 1AIF1 | gene | 1 | — | ◆ | AIF1 is a microglial and macrophage activation marker that drives innate immune responses in atherosclerotic inflammation. | |
| Alpha-1B-GlycoproteinAMBP | protein | 1 | — | ◆ | AMBP modulates complement activation and acute-phase response during atherothrombotic MI. | |
| ARL6IP1ARL6IP1 | gene | 1 | — | ◆ | ARL6IP1 participates in lipid homeostasis and inflammatory signaling during atherosclerotic plaque development. | |
| Aspartylphenylalanine | peptide | 1 | — | — | Dipeptide marker of altered proteolytic and inflammatory metabolism in acute coronary syndrome. | |
| ATP Citrate LyaseACLY | gene | 1 | — | ◆ | ATP citrate lyase controls macrophage acetyl-CoA pools and lipid biosynthesis, influencing the pro-inflammatory versus stabilizing macrophage phenotype in ather | |
| B-cell lymphoma 6BCL6 | protein | 1 | — | ◆ | BCL-6 is an miR-155 target that dampens inflammatory signaling; its suppression permits plaque inflammation amplification. | |
| Bone Morphogenetic Protein 7BMP7 | protein | 1 | — | ◆ | BMP7 exerts cardioprotective effects through suppression of inflammatory pathways and improvement of metabolic dysfunction, reducing atherosclerotic burden. | |
| Bruton Tyrosine KinaseBTK | protein | 1 | — | ◆ | BTK amplifies macrophage activation and lipid uptake into foam cells, accelerating plaque inflammation and destabilization. | |
| BST1BST1 | protein | 1 | — | ◆ | BST1 is involved in oxidative stress and immune cell activation within destabilized atherosclerotic plaques. | |
| Butyrate | metabolite | 1 | — | — | Butyrate exerts cardioprotective effects through histone deacetylase inhibition and reduction of macrophage-driven plaque inflammation. | |
| C-C chemokine receptor type 5CCR5 | protein | 1 | — | ◆ | CCR5 mediates monocyte recruitment into atherosclerotic lesions via CCL3/CCL5 signaling, amplifying plaque inflammation and destabilization. | |
| C-C Motif Chemokine Ligand 21 | protein | 1 | — | — | CCL21 recruits lymphocytes and monocytes to the atherosclerotic lesion, amplifying plaque inflammation. | |
| C-C motif chemokine receptor 8CCR8 | gene | 1 | — | ◆ | Chemokine-receptor mediating monocyte recruitment to the infarcted myocardium and inflammation-driven remodeling. | |
| c-FosFOS | protein | 1 | — | ◆ | c-Fos is an AP-1 subunit activated during plaque inflammation and endothelial response to injury. | |
| C-Reactive Protein, ultrasensitive | protein | 1 | — | — | hs-CRP reflects systemic inflammatory burden from atherosclerotic plaque destabilization and leukocyte infiltration. | |
| C-type lectin domain family 3 member BCLEC3B | protein | 1 | — | ◆ | CLEC3B release from plaques or endothelium during ACS reflects acute vascular inflammation and plaque destabilization. | |
| C-X-C motif chemokine ligand 16CXCL16 | protein | 1 | — | ◆ | CXCL16 recruits inflammatory leukocytes to atherosclerotic plaques, amplifying vascular inflammation. | |
| C-X-C motif chemokine ligand-like factor 1CKLF1 | protein | 1 | — | — | CKLF1 drives monocyte chemotaxis and plaque inflammation, destabilizing atherosclerotic lesions prior to rupture. | |
| C1orf105C1ORF105 | gene | 1 | — | — | C1orf105 is associated with M2 macrophage polarization and plaque inflammatory state in CAD. | |
| CAD238 | peptide | 1 | — | — | CAD238 is a urinary proteomic biomarker associated with coronary artery disease characterization, reflecting chronic vascular inflammation or structural changes | |
| CALB1CALB1 | gene | 1 | — | — | CALB1 calcium-binding protein is associated with M2 macrophage functional programming in plaque inflammation. | |
| cAMP response element binding protein 1CREB1 | protein | 1 | — | — | CREB1 is a transcription factor bridging mitochondrial succinate accumulation to inflammatory gene expression in the atherosclerotic plaque. | |
| CBLBCBLB | gene | 1 | — | ◆ | CBLB regulates acute myocardial infarction through immune cell activation and metabolic responses affecting plaque inflammation and systemic metabolic stress. | |
| CCL9 (Macrophage Inflammatory Protein-1γ)CCL9 | protein | 1 | — | — | Monocyte-recruiting chemokine promoting plaque inflammation and post-infarction ventricular remodeling. | |
| CD11cITGAX | protein | 1 | — | ◆ | CD11c (αX integrin) mediates monocyte adhesion and inflammatory cell recruitment to the destabilized plaque during atherothrombotic MI. | |
| CD14+ microparticles | complex | 1 | — | — | CD14+ microparticles released from activated monocytes carry tissue factor and propagate inflammation and coagulation. | |
| CD30 LigandTNFSF8 | protein | 1 | — | ◆ | CD30 ligand promotes leukocyte activation and vascular inflammation in the atherosclerotic plaque. | |
| CD300LFCD300LF | gene | 1 | — | ◆ | CD300LF regulates immune-cell activation and inflammatory signaling in atherosclerotic plaques. | |
| CD47CD47 | protein | 1 | — | ◆ | CD47 'don't-eat-me' signal suppresses macrophage phagocytosis; altered CD47 expression or signaling modulates plaque inflammation and leukocyte activity. | |
| CD6CD6 | protein | 1 | — | ◆ | CD6 promotes T-cell recruitment and inflammatory activation in coronary atherosclerotic plaque. | |
| CD69 AntigenCD69 | protein | 1 | — | ◆ | CD69 marks early T cell activation and leukocyte recruitment during acute coronary thrombosis and myocardial injury. | |
| CD82CD82 | gene | 1 | — | ◆ | CD82 mediates cell–cell adhesion and inflammatory-cell recruitment, contributing to leukocyte infiltration and vascular inflammation in plaque. | |
| Cell Migration Inducing hyaluronan Binding ProteinCEMIP | gene | 1 | — | ◆ | CEMIP expression is induced during atherosclerotic plaque development and contributes to vascular inflammation and plaque progression. | |
| ceramide C24:1/C24:0 | lipid | 1 | — | — | Ceramide C24:1/C24:0 is a pro-inflammatory sphingolipid that activates endothelial dysfunction and vascular inflammation, contributing to atherosclerotic plaque | |
| Chemokine (C-C motif) ligand 6CCL6 | gene | 1 | — | — | CCL6 recruits B cells into the post-MI inflammatory microenvironment. | |
| CKAP4CKAP4 | gene | 1 | — | ◆ | CKAP4 expression differentiates inflammatory phenotypes in diabetic coronary artery disease. | |
| CLEC4DCLEC4D | protein | 1 | — | ◆ | CLEC4D is a core gene shared between ischemic stroke and MI; regulates myeloid-cell activation and inflammatory responses in atherothrombosis. | |
| CLEC4ECLEC4E | gene | 1 | — | ◆ | CLEC4E promotes monocyte and macrophage recruitment and activation in atherosclerotic plaques, driving inflammation and rupture susceptibility. | |
| CLEC5ACLEC5A | gene | 1 | — | ◆ | CLEC5A enhances monocyte and neutrophil innate immune signaling, intensifying plaque inflammation and thrombotic activation in acute MI. | |
| CLEC7ACLEC7A | protein | 1 | — | ◆ | CLEC7A promotes monocyte/macrophage recruitment and oxidative enzyme release driving plaque inflammation. | |
| Cluster of Differentiation 4CD4 | protein | 1 | — | ◆ | CD4+ T cells infiltrate and drive pro-inflammatory responses within atherosclerotic plaques. | |
| Cluster of Differentiation 74CD74 | gene | 1 | — | ◆ | CD74 is the MIF-2 signaling receptor, mediating macrophage activation and plaque inflammation. | |
| Colony Stimulating Factor 1 ReceptorCSF1R | gene | 1 | — | ◆ | CSF1R drives monocyte/macrophage recruitment and survival in atherosclerotic plaque inflammation. | |
| Complement C1q subcomponent subunit CC1QC | protein | 1 | — | ◆ | C1QC expression marks plaque macrophage activation and complement-mediated inflammation contributing to atherosclerotic lesion progression. | |
| Complement C1r serine proteaseC1R | protein | 1 | — | — | C1R initiates complement cascade amplifying inflammation and macrophage recruitment in unstable plaques. | |
| Complement C1r-like Serine ProteaseC1RL | protein | 1 | — | ◆ | C1RL initiates classical-complement cascade, and its decreased level may reflect complement consumption during acute MI. | |
| Complement C8BC8B | protein | 1 | — | ◆ | C8B, part of the complement membrane-attack complex, participates in plaque inflammation and vascular injury during acute coronary syndrome. | |
| Complement Component 4BC4B | protein | 1 | — | ◆ | C4B complement cascade activation recruits inflammatory cells to destabilize atherosclerotic plaques. | |
| Complement component C9C9 | protein | 1 | — | ◆ | C9 participates in complement-mediated inflammatory activation, promoting plaque inflammation and platelet-leukocyte aggregation. | |
| Complement Factor BCFB | protein | 1 | — | ◆ | CFB participates in complement-mediated inflammation downstream of IL-6R signaling in atherosclerotic plaques. | |
| CRYGBCRYGB | gene | 1 | — | — | CRYGB is associated with M2 macrophage polarization and inflammatory remodeling in coronary plaques. | |
| CTHRC1CTHRC1 | gene | 1 | — | ◆ | CTHRC1 marks activated fibroblasts driving extracellular matrix remodeling and plaque inflammation. | |
| Cyclin-Dependent Kinase 7CDK7 | gene | 1 | — | ◆ | CDK7 regulates inflammatory gene expression and cell proliferation in plaque-resident immune and vascular cells. | |
| Cystic Fibrosis Transmembrane Conductance RegulatorCFTR | protein | 1 | — | ◆ | CFTR dysfunction impairs sphingosine-1-phosphate degradation, exacerbating post-MI inflammation. | |
| Cytotoxic T-Lymphocyte Antigen 4CTLA4 | gene | 1 | — | ◆ | CTLA4 suppresses T-cell co-stimulation post-MI, reducing excessive adaptive immune inflammation and plaque destabilization. | |
| DEAF1 transcription factorDEAF1 | gene | 1 | — | ◆ | DEAF1 controls transcriptional programs of immune tolerance that limit pathologic post-MI inflammation. | |
| Defensin Alpha 1DEFA1 | protein | 1 | — | ◆ | DEFA1 (human neutrophil defensin) is released by activated neutrophils and marks acute plaque inflammation and thrombotic risk. | |
| Defensin Beta 127DEFB127 | gene | 1 | — | ◆ | DEFB127 bridges diabetes-related immune dysfunction and coronary artery disease susceptibility via innate immune mechanisms. | |
| Dickkopf-3DKK3 | protein | 1 | — | ◆ | DKK3 inhibits Wnt signaling to suppress inflammation and promote matrix remodeling during plaque destabilization. | |
| DNA Methyltransferase 1DNMT1 | gene | 1 | — | ◆ | DNMT1 maintains DNA methylation patterns controlling expression of miR-520e and inflammatory mediators in atherosclerotic plaque cells. | |
| DNA-myeloperoxidase complexes | other | 1 | — | — | DNA-MPO complexes released by activated neutrophils form prothrombotic nets that amplify both plaque inflammation and thrombotic responses in Type 1 MI. | |
| DNAJB6DNAJB6 | gene | 1 | — | — | DNAJB6 regulates protein folding and cellular stress responses affecting macrophage and endothelial function in atherosclerotic plaques. | |
| DNASE1DNASE1 | gene | 1 | — | ◆ | DNASE1 polymorphisms affecting NET degradation alter neutrophil-mediated plaque inflammation and thrombotic burden in MI. | |
| DPEP1DPEP1 | protein | 1 | — | ◆ | DPEP1 is a circulating protein linked to elevated myocardial infarction risk through pathways not yet fully characterized. | |
| DSCAML1DSCAML1 | protein | 1 | — | ◆ | DSCAML1 promotes leukocyte recruitment and endothelial activation in coronary plaque inflammation. | |
| EEQs | metabolite | 1 | — | — | EEQs dampen pro-inflammatory cytokine signaling and platelet function, reducing atherothrombotic progression. | |
| Eotaxin (CCL11)CCL11 | protein | 1 | — | ◆ | Chemokine recruiting eosinophils and monocytes to inflamed coronary plaque during acute STEMI. | |
| ERV1 (Resolvin E1 receptor) | protein | 1 | — | — | ERV1 signaling suppresses macrophage activation and inflammatory cytokine production, stabilizing the atherosclerotic plaque. | |
| Esterified hydroxyeicosatetraenoic acids | lipid | 1 | — | — | Esterified oxidized eicosanoid metabolites generated during plaque inflammation that characterize vulnerable, symptomatic atherosclerotic lesions. | |
| FAM5CFAM5C | gene | 1 | — | — | FAM5C promotes smooth-muscle-cell proliferation and vascular remodeling, contributing to atherosclerotic plaque growth and structural instability. | |
| Fas LigandFASLG | gene | 1 | — | ◆ | FASLG upregulation modulates inflammatory cell apoptosis and immune activation in plaque destabilization. | |
| Ferritin light chainFTL | protein | 1 | — | ◆ | Ferritin light chain reflects iron-catalyzed oxidative stress and inflammatory burden in atherosclerotic plaque destabilization. | |
| FHL3FHL3 | gene | 1 | — | — | FHL3 is a CAD-variant-regulated smooth muscle gene that modulates vascular inflammation and structural adaptation in atherosclerosis. | |
| FOXP3FOXP3 | gene | 1 | — | — | FOXP3 hypermethylation impairs regulatory T cell function, promoting plaque inflammation and atherothrombotic progression. | |
| FPR2FPR2 | gene | 1 | — | ◆ | FPR2 mediates neutrophil and monocyte chemotaxis, amplifying plaque inflammation and destabilization. | |
| FRKFRK | gene | 1 | — | ◆ | FRK regulates macrophage activation and integrin signaling in atherosclerotic plaque inflammation. | |
| Galectin-3-Binding ProteinLGALS3BP | protein | 1 | — | ◆ | LGALS3BP associates with plaque inflammation and matrix remodeling, reflecting macrophage activity and cap vulnerability. | |
| Galectin-9LGALS9 | gene | 1 | — | ◆ | LGALS9 controls macrophage infiltration into atherosclerotic plaques through CD44-mediated interactions. | |
| Ganglioside GM3 | lipid | 1 | — | — | GM3 ganglioside modulates immune cell and platelet activation during atherosclerotic plaque inflammation and thrombotic responses. | |
| GAP43GAP43 | protein | 1 | — | ◆ | GAP43 is associated with M2 macrophage polarization and neuronal-immune crosstalk in plaque inflammation. | |
| glucosylceramide | lipid | 1 | — | — | Glucosylceramide modulates inflammatory responses within atherosclerotic plaques, supporting plaque stability. | |
| GLULGLUL | gene | 1 | — | ◆ | GLUL participates in glutamic acid metabolism, supporting inflammatory pathways implicated in coronary atherosclerotic disease. | |
| Glyoxalase IGLO1 | gene | 1 | — | ◆ | GLO1 regulates detoxification and antigen processing, modulating immune responses in plaque inflammation. | |
| Granulocyte chemotactic protein 2 (CXCL6)CXCL6 | protein | 1 | — | ◆ | Neutrophil-recruiting chemokine amplifying acute plaque inflammation and post-MI remodeling. | |
| GTP Cyclohydrolase IGCH1 | gene | 1 | — | ◆ | GTP cyclohydrolase I sustains nitric oxide production in endothelium, preserving vasodilation and reducing plaque inflammation and endothelial activation. | |
| GTPase IMAP Family Member 6GIMAP6 | protein | 1 | — | — | GIMAP6 regulates immune cell survival and function, influencing post-MI inflammatory state. | |
| GTPase IMAP Family Member 7GIMAP7 | protein | 1 | — | ◆ | GIMAP7 regulates immune cell survival and function, influencing post-MI inflammatory state. | |
| H19H19 | rna | 1 | — | — | H19 circulating levels reflect apoptosis-autophagy signaling in plaque macrophages, integrating inflammation and matrix destabilization. | |
| HBP1HBP1 | gene | 1 | — | — | HBP1 regulates inflammatory and proliferative transcriptional programs during atherosclerotic plaque evolution. | |
| HDHD2HDHD2 | protein | 1 | — | ◆ | HDHD2 functions as a circulating protective factor reducing myocardial infarction risk, likely through anti-inflammatory or lipid-modulating activity. | |
| HFAT4 | rna | 1 | — | — | HFAT4 promotes anti-inflammatory monocyte differentiation reducing plaque destabilization. | |
| histone deacetylase | protein | 1 | — | — | HDAC modulates epigenetic regulation of inflammatory gene expression in cardiac ischemia and atherosclerosis. | |
| HLA-BHLA-B | gene | 1 | — | ✦◆ | HLA-B is a causal target for oxidative stress-linked CAD, influencing immune-cell recruitment and plaque inflammation. | |
| HLA-DQA1HLA-DQA1 | gene | 1 | — | ◆ | HLA-DQA1 drives adaptive immune activation and antigen presentation, promoting chronic plaque inflammation that destabilizes the atherosclerotic lesion. | |
| HLA-DRB1HLA-DRB1 | gene | 1 | — | ◆ | HLA-DRB1 drives adaptive immune activation and antigen presentation, promoting chronic plaque inflammation that destabilizes the atherosclerotic lesion. | |
| HLA-GHLA-G | gene | 1 | — | ◆ | HLA-G, a non-classical MHC molecule, modulates immune tolerance and inflammation, influencing atherosclerotic plaque progression and stability. | |
| IgG autoantibodies to oxidized LDL | protein | 1 | — | — | IgG autoantibodies to oxidized LDL amplify inflammatory responses to atherogenic lipid modification and plaque destabilization. | |
| IgM autoantibodies to oxidized LDL | protein | 1 | — | — | IgM autoantibodies to oxidized LDL exert atheroprotective effects by suppressing pro-inflammatory immune responses to atherogenic LDL oxidation. | |
| IL-8 Receptor Type 1CXCR1 | protein | 1 | — | ◆ | IL-8R1 mediates neutrophil infiltration and oxidative damage in inflamed coronary atherosclerotic plaques. | |
| Inducible T Cell Co-stimulatorICOS | protein | 1 | — | ◆ | ICOS-mediated T cell costimulation intensifies the adaptive inflammatory response during acute myocardial infarction. | |
| Inducible T-cell costimulatory ligandICOSLG | protein | 1 | — | ◆ | ICOSLG expression on antigen-presenting cells amplifies T-cell-driven plaque inflammation and destabilization. | |
| Inhibitor of κB kinaseIKBKG | protein | 1 | — | ◆ | IKK-mediated NF-κB activation drives pro-inflammatory cytokine production and macrophage recruitment within destabilizing plaques. | |
| INPP5BINPP5B | gene | 1 | — | ◆ | INPP5B is a CAD-variant-regulated gene in smooth muscle cells that influences atherosclerotic plaque development through vascular remodeling. | |
| Integrin Beta-7ITGB7 | protein | 1 | — | ◆ | ITGB7 integrin mediates adhesion of leukocytes to inflamed endothelium and vascular tissue in acute coronary syndrome. | |
| Intelectin-1ITLN1 | gene | 1 | — | ◆ | ITLN1 modulates innate immune responses and metabolic inflammation linked to atherosclerotic risk. | |
| Interferon Induced with Helicase C Domain 1IFIH1 | gene | 1 | — | ◆ | IFIH1 is a viral RNA sensor that triggers innate immunity and pro-inflammatory responses implicated in atherosclerotic inflammation. | |
| Interferon-alpha 2IFNA2 | gene | 1 | — | ◆ | Interferon-alpha drives type-1 interferon-mediated vascular inflammation contributing to plaque destabilization. | |
| Interleukin-13IL13 | protein | 1 | — | ◆ | IL-13 promotes alternative macrophage activation and fibrosis, providing atheroprotection against plaque rupture. | |
| Interleukin-18 receptor 1IL18R1 | protein | 1 | — | ◆ | IL-18 receptor mediating inflammatory signaling in atherosclerotic plaque and post-MI myocardial remodeling. | |
| Interleukin-19IL19 | protein | 1 | — | ◆ | IL-19 exerts anti-inflammatory effects that may suppress atherosclerotic plaque development and inflammation. | |
| Interleukin-20IL20 | protein | 1 | — | ◆ | IL-20 drives pro-inflammatory signaling within atherosclerotic plaques, contributing to their inflammatory microenvironment. | |
| Interleukin-27IL27 | protein | 1 | — | ◆ | IL-27 exerts immunomodulatory and cardioprotective effects that suppress inflammatory responses in atherosclerosis and myocardial injury. | |
| Interleukin-32IL32 | protein | 1 | — | ◆ | IL-32 is a pro-inflammatory cytokine that amplifies atherosclerotic plaque inflammation. | |
| Interleukin-36IL36G | protein | 1 | — | ◆ | IL-36 cytokine family member promoting vascular inflammation and atherosclerotic plaque destabilization. | |
| Interleukin-8IL8 | protein | 1 | — | — | IL-8 recruits neutrophils and monocytes to atherosclerotic plaque, amplifying vascular inflammation and destabilization. | |
| Itaconic acid | metabolite | 1 | — | — | Itaconic acid elevation reflects macrophage activation and inflammatory immune metabolism during acute infarction. | |
| JNK1MAPK8 | protein | 1 | — | ◆ | c-Jun N-terminal kinase-1 amplifies vascular inflammation and platelet activation during plaque destabilization. | |
| KAT1KAT1 | gene | 1 | — | — | KAT1 upregulation in macrophages during acute myocardial infarction reflects kynurenine pathway activation and plaque inflammation. | |
| KIR2DS2KIR2DS2 | protein | 1 | — | — | KIR2DS2 may protect against MI by suppressing excessive plaque inflammation via NK-cell signaling. | |
| KLC1KLC1 | gene | 1 | — | ◆ | KLC1 influences intracellular signaling and inflammatory cell transport, with pleiotropic effects on atherogenic pathways. | |
| KPNA2KPNA2 | gene | 1 | — | — | KPNA2 regulates nuclear translocation of inflammatory transcription factors, potentially modulating monocyte and endothelial inflammatory responses. | |
| Kynurenine | metabolite | 1 | — | — | Kynurenine, produced by IDO1 in thrombi macrophages, amplifies innate immune activation and vascular inflammation in STEMI pathogenesis. | |
| L-kynurenine | metabolite | 1 | — | — | L-kynurenine, a tryptophan catabolite, is elevated in acute MI with renal comorbidity and signals inflammatory immune activation. | |
| LAYNLAYN | gene | 1 | — | ◆ | LAYN regulates immune cell adhesion and trafficking, with protective effects against excessive plaque inflammation and atherothrombotic progression. | |
| Leukocyte-derived microparticles | complex | 1 | — | — | Leukocyte-derived vesicles released during monocyte/neutrophil activation, linking inflammation to thrombotic cascade. | |
| Leukotriene A4 hydrolaseLTA4H | protein | 1 | — | ◆ | LTA4H catalyzes leukotriene production, amplifying neutrophil recruitment to the atherosclerotic lesion and promoting plaque inflammation and thrombotic respons | |
| leukotriene C4 | metabolite | 1 | — | — | Leukotriene C4 is an eicosanoid inflammatory mediator released during leukocyte and platelet activation in ACS. | |
| LIMS1LIMS1 | gene | 1 | — | ◆ | LIMS1 modulates integrin signaling and cellular adhesion during plaque inflammation and leukocyte recruitment. | |
| LINC00968LINC00968 | rna | 1 | — | — | Long non-coding RNA dysregulated in coronary artery disease and epicardial adipose tissue, likely modulating vascular inflammation. | |
| LPC 17:0 | lipid | 1 | — | — | LPC 17:0 elevation in myocardial infarction reflects both lipid remodeling and systemic inflammatory activation. | |
| LRP1BLRP1B | protein | 1 | — | ◆ | LRP1B participates in lipoprotein homeostasis and inflammatory signaling during atherothrombotic plaque destabilization. | |
| LRRFIP1LRRFIP1 | gene | 1 | — | ◆ | LRRFIP1 participates in innate immune signaling affecting atherosclerotic plaque inflammation. | |
| LY96LY96 | gene | 1 | — | ◆ | LY96 amplifies TLR-mediated monocyte and endothelial activation, intensifying plaque inflammation and atherothrombotic susceptibility. | |
| Lymphotactin (XCL1)XCL1 | protein | 1 | — | ◆ | Chemokine mediating lymphocyte recruitment in plaque inflammation and post-MI ventricular remodeling. | |
| Lysoalkylphosphatidylcholine | lipid | 1 | — | — | Lysoalkylphosphatidylcholine is a pro-inflammatory lipid mediator in dense LDL promoting vascular inflammation. | |
| Lysolipids | lipid | 1 | — | — | Lysolipids generated from lipoprotein remodeling act as endothelial and immune-cell activators, driving plaque inflammation. | |
| Lysophosphatidylinositol | lipid | 1 | — | — | Lysophosphatidylinositol is a pro-inflammatory lipid mediator carried in dense LDL that amplifies plaque inflammation. | |
| Macrophage Stimulating Protein 1MST1 | protein | 1 | — | — | MST1 enhances macrophage recruitment and inflammatory activation within the atherosclerotic plaque. | |
| Mannan-binding Lectin Associated Serine Protease 1MASP1 | protein | 1 | — | ◆ | MASP1 activates the lectin-complement pathway, driving plaque inflammation and cross-talk with coagulation. | |
| Mannosidase Alpha Class 1A Member 1MAN1A1 | protein | 1 | — | ◆ | MAN1A1 participates in inflammatory response pathways activated during myocardial infarction and ischemic injury. | |
| MAP3K7CLMAP3K7CL | gene | 1 | — | — | MAP3K7CL regulates kinase signaling in smooth-muscle cells, potentially modulating inflammatory responses in atherosclerosis. | |
| MCEMP1MCEMP1 | gene | 1 | — | ◆ | MCEMP1 expression reflects mast-cell degranulation and vascular inflammation, contributing to plaque destabilization and thrombotic activation. | |
| MCP-4 (CCL8)CCL8 | protein | 1 | — | ◆ | Monocyte-recruiting chemokine amplifying acute inflammatory response in STEMI plaque rupture. | |
| Methionine sulfoxide | metabolite | 1 | — | — | Methionine sulfoxide is an oxidized amino acid product reflecting oxidative stress and plaque inflammation in acute myocardial infarction. | |
| Methionine Sulfoxide Reductase AMSRA | gene | 1 | — | — | Methionine sulfoxide reductase A reduces oxidative stress in atherosclerotic plaques and ischemic myocardium, limiting inflammation-driven plaque destabilizatio | |
| MIA3MIA3 | gene | 1 | — | ✦◆ | MIA3 downstream of ADTRP modulates leukocyte adhesion molecule trafficking and endothelial activation, reducing plaque inflammation. | |
| microRNA-155MIR155 | rna | 1 | — | — | miR-155 promotes vascular inflammation and plaque destabilization by suppressing anti-inflammatory targets (BCL-6, STAT-3) and enhancing monocyte/macrophage inf | |
| microRNA-17 | rna | 1 | — | — | A microRNA regulating inflammatory pathways in acute coronary syndrome, controlling immune cell activation and vascular inflammation. | |
| microRNA-660 | rna | 1 | — | — | A microRNA modulating MI severity through regulation of inflammatory and cardiomyocyte injury pathways. | |
| MidkineMDK | protein | 1 | — | ◆ | Midkine amplifies post-MI myocardial inflammation and adverse remodeling through growth-factor signaling on the plaque-inflammation and systemic-response axes. | |
| miR-1307-5p | rna | 1 | — | — | miRNA marking plaque inflammation and vascular dysfunction in acute coronary syndrome. | |
| miR-130a | rna | 1 | — | — | miR-130a modulates inflammatory signaling in atherosclerotic plaque. | |
| miR-130a-3p | rna | 1 | — | — | miR-130a-3p dysregulation impairs endothelial function and promotes vascular inflammation in coronary artery disease pathogenesis. | |
| miR-130b-5p | rna | 1 | — | — | Circulating microRNA modulating inflammatory and matrix-remodeling pathways associated with atherosclerotic plaque severity. | |
| miR-146a | rna | 1 | — | — | miR-146a modulates innate immune and inflammatory signaling in plaque destabilization. | |
| miR-146a-5p | rna | 1 | — | — | miR-146a-5p regulates inflammatory cytokine signaling during acute coronary syndromes, enabling ACS detection via plaque inflammation. | |
| miR-18a-3p | rna | 1 | — | — | Circulating microRNA regulating inflammatory and lipid-metabolic gene networks dysregulated in coronary artery disease. | |
| miR-20b-5p | rna | 1 | — | — | miR-20b-5p regulates osteopontin and inflammatory pathways in myocardial remodeling after MI. | |
| miR-223-5p | rna | 1 | — | — | miR-223-5p modulates myeloid cell activation and inflammatory responses associated with coronary artery disease. | |
| miR-2861 | rna | 1 | — | — | Circulating miRNA dysregulated in acute coronary syndrome with roles in inflammation and ischemic injury. | |
| miR-320a | rna | 1 | — | — | miR-320a regulates osteopontin expression and inflammatory responses in atherothrombotic injury. | |
| miR-320b | rna | 1 | — | — | miR-320b regulates osteopontin and inflammatory signaling in post-MI myocardial remodeling. | |
| miR-320d | rna | 1 | — | — | miR-320d regulates osteopontin expression and inflammatory pathways in atherothrombotic injury. | |
| miR-326 | rna | 1 | — | — | miR-326 is a circulating biomarker dysregulated in CAD, modulating inflammatory and lipid-metabolism pathways in atherosclerotic plaque. | |
| miR-378a-3p | rna | 1 | — | — | miR-378a-3p regulates osteopontin and inflammatory remodeling pathways in post-MI myocardial injury. | |
| miR-520e | rna | 1 | — | — | miR-520e is downregulated during acute coronary syndrome and inhibits cell-proliferation pathways relevant to plaque destabilization. | |
| miR-720 | rna | 1 | — | — | Circulating miRNA dysregulated in acute coronary syndrome, reflecting inflammatory and myocardial-injury mechanisms. | |
| miR-802 | rna | 1 | — | — | miR-802 upregulation amplifies endothelial inflammation and plaque destabilization in Type 1 MI, particularly in MINOCA phenotypes. | |
| miR-92 | rna | 1 | — | — | Circulating miRNA with roles in endothelial dysfunction and inflammation, predictive of acute coronary syndrome. | |
| Mitochondrial transcription factor ATFAM | protein | 1 | — | ◆ | Mitochondrial transcription factor A released as a damage-associated molecular pattern promotes plaque inflammation and atherosclerotic progression. | |
| Mitogen-Activated Protein Kinase Kinase Kinase 14MAP3K14 | gene | 1 | — | ◆ | MAP3K14 activates non-canonical NF-κB signaling in plaque macrophages and vascular inflammation. | |
| Monomeric C-reactive protein | protein | 1 | — | — | mCRP drives plaque inflammation and is elevated in acute MI, reflecting inflammatory activation. | |
| MSMPMSMP | gene | 1 | — | ◆ | MSMP has putative roles in immune regulation and vascular remodeling with uncertain mechanistic links to atherothrombotic MI pathogenesis. | |
| Murinoglobulin-1MUG1 | protein | 1 | — | — | MUG1 inhibits neutrophil serine protease release, dampening post-MI inflammatory injury. | |
| MyD88MYD88 | protein | 1 | — | ◆ | MyD88 transduces toll-like-receptor signals that drive monocyte recruitment and vascular inflammation destabilizing atherosclerotic plaques. | |
| N-lactoyl-phenylalanine | metabolite | 1 | — | — | N-lactoyl-phenylalanine is a metabolite of mitochondrial dysfunction and inflammation associated with acute myocardial infarction risk. | |
| N6-methyladenosine | metabolite | 1 | — | — | N6-methyladenosine modulates mRNA stability of atherosclerosis-related genes. | |
| NADPH oxidase | gene | 1 | — | — | NOX-mediated ROS production drives endothelial activation and inflammatory cell recruitment; its inhibition supports endothelial progenitor repair. | |
| NADPH oxidase 2CYBB | gene | 1 | — | ◆ | NOX2-catalyzed superoxide production oxidizes retained lipoproteins and amplifies inflammatory monocyte/macrophage recruitment in the atherosclerotic plaque. | |
| NAGLUNAGLU | gene | 1 | — | ◆ | NAGLU is a causal target for oxidative stress-linked CAD contributing to plaque inflammation and atherosclerotic progression. | |
| NCF2NCF2 | gene | 1 | — | ◆ | NCF2 encodes p67phox, a core NADPH-oxidase subunit generating superoxide in activated macrophages and destabilizing plaques. | |
| NEAT1NEAT1 | rna | 1 | — | — | NEAT1 modulates inflammatory gene expression and plaque stability through interaction with paraspeckle proteins. | |
| NF-kappa-B Inhibitor AlphaNFKBIA | gene | 1 | — | ◆ | NFKBIA restrains NF-κB-mediated inflammatory signaling in atherosclerotic plaque development. | |
| NRIP3NRIP3 | gene | 1 | — | — | NRIP3 is a CAD-variant-regulated gene in smooth muscle that modulates inflammatory and metabolic responses in atherosclerosis. | |
| Nuclear Factor Interleukin 3 RegulatedNFIL3 | gene | 1 | — | — | NFIL3 is a transcriptional regulator of innate lymphoid cell and NK cell differentiation, implicated in CAD-associated immune dysregulation. | |
| Oncostatin M ReceptorOSMR | protein | 1 | — | ◆ | OSMR mediates IL-6 receptor trans-signaling that promotes vascular inflammation and atherosclerotic plaque destabilization. | |
| ORMDL3ORMDL3 | gene | 1 | — | ◆ | ORMDL3 regulates sphingolipid metabolism and innate immune signaling, modulating plaque inflammation in atherothrombosis. | |
| P2X7 ReceptorP2RX7 | protein | 1 | — | ◆ | P2X7 receptor activation on neutrophils and macrophages amplifies plaque inflammation through inflammatory mediator release. | |
| P2Y Purinergic Receptor 14P2RY14 | gene | 1 | — | ◆ | P2RY14 is an immune response receptor that regulates inflammatory cytokine production during atherosclerotic plaque inflammation. | |
| PAX8-AS1 | rna | 1 | — | — | PAX8-AS1 regulates miR-15a-5p expression in endothelial cells, modulating inflammatory responses in acute coronary syndrome. | |
| PDK4PDK4 | gene | 1 | — | ◆ | PDK4 expression in neutrophils promotes glycolytic metabolism supporting NETosis and neutrophil-driven plaque inflammation. | |
| Peptidoglycan recognition protein 2PGLYRP2 | protein | 1 | — | ◆ | Innate immune sensor whose altered expression in STEMI amplifies plaque-destabilizing inflammation and monocyte recruitment. | |
| Peroxiredoxin-4PRDX4 | protein | 1 | — | ◆ | Antioxidant peroxiredoxin that suppresses lipid oxidation and plaque inflammation; reduced activity promotes atherothrombotic progression. | |
| PFKFB3PFKFB3 | gene | 1 | — | ◆ | PFKFB3 upregulation couples glycolytic metabolism to inflammatory macrophage activation, amplifying plaque destabilization. | |
| PFKLPFKL | gene | 1 | — | ◆ | PFKL methylation and expression regulate neutrophil glycolysis and inflammatory activation in atherothrombotic disease. | |
| Phospholipase A2 Group IIDPLA2G2D | gene | 1 | — | ◆ | Secreted phospholipase regulating immune response and lipid mediator synthesis in atherosclerotic plaque inflammation. | |
| Phospholipase A2 group IIIPLA2G3 | gene | 1 | — | ◆ | Phospholipase A2 isoform generating pro-inflammatory lipid mediators and oxidized phospholipids during atherosclerotic plaque inflammation. | |
| PIK3R3PIK3R3 | gene | 1 | — | ◆ | PIK3R3 downstream of ADTRP inhibits monocyte-endothelial adhesion and recruitment, suppressing plaque-destabilizing inflammation. | |
| PILRAPILRA | gene | 1 | — | ◆ | PILRA regulates innate immune activation and monocyte/macrophage function in atherosclerotic plaque inflammation. | |
| Polyhomeotic Chromodomain-like Protein 2 (PHC2 / EDR1)PHC2 | gene | 1 | — | — | PHC2 expression dysregulation modulates immune cell activation in acute MI inflammation. | |
| Polymeric immunoglobulin receptorPIGR | protein | 1 | — | ◆ | Immunoglobulin receptor present in circulating microvesicles; elevation during ACS indicates endothelial activation and inflammatory vascular response. | |
| PRMT9PRMT9 | gene | 1 | — | ◆ | PRMT9-mediated arginine methylation of PFKL and other substrates controls neutrophil activation and NET formation during coronary thrombosis. | |
| Pro-substance P | peptide | 1 | — | — | Pro-substance P amplifies vascular inflammation and platelet activation, increasing post-MI adverse-event risk. | |
| Programmed cell death protein 1PDCD1 | protein | 1 | — | ◆ | PD-1 signaling modulates plaque-infiltrating T-cell exhaustion and inflammation, influencing plaque stability and rupture susceptibility. | |
| Programmed death-ligand 1CD274 | protein | 1 | — | ◆ | PD-L1 expression by macrophages and endothelial cells suppresses protective T-cell responses, promoting chronic plaque inflammation and instability. | |
| ProhibitinPHB | protein | 1 | — | — | Prohibitin limits oxidative stress and inflammatory signaling in atherosclerotic plaque. | |
| Prostaglandin D | metabolite | 1 | — | — | Elevated prostaglandin D in atherosclerotic aorta reflects increased eicosanoid-driven inflammatory activation of the plaque. | |
| Prostaglandin D synthasePTGDS | protein | 1 | — | ◆ | Prostaglandin D synthase participates in eicosanoid-mediated plaque inflammation and platelet modulation during atherothrombotic rupture. | |
| Prostaglandin J2 | metabolite | 1 | — | — | PGJ2 promotes monocyte infiltration and inflammatory cytokine production, destabilizing the atherosclerotic plaque. | |
| Protease-activated receptor 2F2RL1 | protein | 1 | — | ◆ | PAR-2 activation by trypsin amplifies vascular inflammation and monocyte/macrophage infiltration destabilizing the atherosclerotic plaque. | |
| Protein phosphatase 2 regulatory subunit 3APPP2R3A | protein | 1 | — | ✦ | PPP2R3A modulates phosphatase activity in inflammatory pathways implicated in coronary atherothrombotic disease. | |
| Protein phosphatase 5PPP5C | protein | 1 | — | ◆ | Protein phosphatase 5 controls leukotriene B4 production by regulating 5-lipoxygenase phosphorylation, amplifying inflammatory cell recruitment to the plaque. | |
| Protein Tyrosine Phosphatase Nonreceptor Type 6PTPN6 | gene | 1 | — | ◆ | PTPN6 modulates immune cell activation in acute myocardial injury. | |
| PSMB8-AS1PSMB8-AS1 | rna | 1 | — | — | Long non-coding RNA dysregulated in acute coronary syndrome with inflammatory and injury-associated roles. | |
| PTPN21PTPN21 | protein | 1 | — | — | PTPN21 phosphatase regulates macrophage signaling and M2 polarization in atherosclerotic plaque inflammation. | |
| PTPRCPTPRC | gene | 1 | — | ◆ | PTPRC (CD45) is a leukocyte-signaling hub gene dysregulated in acute MI with concurrent chronic renal failure. | |
| PU.1SPI1 | gene | 1 | — | ◆ | PU.1 controls myeloid and macrophage differentiation programs central to atherosclerotic inflammation and lipid handling. | |
| PYHIN1PYHIN1 | protein | 1 | — | — | PYHIN1 is a pattern-recognition innate immune sensor; smoking-associated variants modulate inflammatory response in AMI. | |
| Receptor for Advanced Glycation End ProductsAGER | protein | 1 | — | ◆ | AGER (RAGE) mediates recognition of advanced glycation end products and oxidized lipids, amplifying plaque inflammation and endothelial dysfunction. | |
| REG1PREG1P | gene | 1 | — | — | REG1P is associated with M2 macrophage programming and inflammatory remodeling in atherosclerotic plaques. | |
| REL proto-oncogeneREL | gene | 1 | — | — | REL is an NF-κB family member driving post-MI T cell and immune activation. | |
| Resolvin E1 | metabolite | 1 | — | — | Resolvin E1 dampens monocyte/macrophage recruitment and cytokine production, promoting plaque stabilization. | |
| Retinoid-related orphan receptor gamma-tRORC | protein | 1 | — | ◆ | RORγt directs Th17 differentiation and IL-17 secretion, amplifying plaque inflammation and destabilization. | |
| RNAS6RNAS6 | protein | 1 | — | — | RNAS6 participates in vascular inflammation and fibrotic remodeling associated with atherosclerotic plaque progression. | |
| RP11-247A12.1 | rna | 1 | — | — | RP11-247A12.1 circulating levels reflect macrophage apoptosis and autophagy dysregulation in destabilizing atherosclerotic plaques. | |
| RP11-288L9.4 | rna | 1 | — | — | Circulating lncRNA regulating apoptosis and autophagy pathways implicated in atherosclerotic plaque destabilization and myocardial injury. | |
| RP11-344B5.2 | rna | 1 | — | — | Circulating lncRNA regulating apoptosis and autophagy pathways implicated in atherosclerotic plaque destabilization and myocardial injury. | |
| RP11-452C8.1 | rna | 1 | — | — | Circulating lncRNA regulating apoptosis and autophagy pathways implicated in atherosclerotic plaque destabilization and myocardial injury. | |
| RP11-565A3.1 | rna | 1 | — | — | Circulating lncRNA regulating apoptosis and autophagy pathways implicated in atherosclerotic plaque destabilization and myocardial injury. | |
| RP5-1114G22.2 | rna | 1 | — | — | RP5-1114G22.2 circulating levels reflect macrophage apoptosis and autophagy dysregulation in destabilizing atherosclerotic plaques. | |
| RP5-902P8.10 | rna | 1 | — | — | RP5-902P8.10 circulating levels reflect macrophage apoptosis and autophagy dysregulation in destabilizing atherosclerotic plaques. | |
| RPTORRPTOR | gene | 1 | — | ◆ | RPTOR is a causal target linking oxidative stress and mTOR-driven metabolic dysregulation to plaque inflammation and atherothrombosis. | |
| S100A4S100A4 | protein | 1 | — | ◆ | Alarmin driving macrophage-mediated plaque inflammation and structural instability. | |
| S100A6S100A6 | protein | 1 | — | ◆ | S100A6 mediates monocyte/macrophage recruitment and inflammatory signaling destabilizing atherosclerotic plaque. | |
| Secretoglobin family 3A member 2SCGB3A2 | protein | 1 | — | ◆ | SCGB3A2 modulates plaque inflammation and endothelial activation in atherothrombotic lesions during STEMI pathogenesis. | |
| Semaphorin-3BSEMA3B | protein | 1 | — | ◆ | Pericoronary SEMA3B dysregulation drives vascular inflammation and endothelial dysfunction contributing to atherosclerotic plaque development. | |
| Signal Transducer and Activator of Transcription 5STAT5 | protein | 1 | — | — | STAT5 signaling propagates T cell activation and cytokine production during acute myocardial infarction inflammation. | |
| Signal Transducer and Activator of Transcription 6STAT6 | protein | 1 | — | ◆ | STAT6 modulates Th2 immunity and vascular inflammation in SCAD pathogenesis. | |
| SMAD Family Member (Canonical TGF-β Signaling) | protein | 1 | — | — | SMAD signaling regulates fibrotic and inflammatory remodeling of the atherosclerotic plaque and fibrous cap. | |
| Small Nucleolar RNA C/D Box 113-2SNORD113-2 | rna | 1 | — | — | SNORD113-2 regulates ribosomal and protein maturation pathways implicated in cardiovascular inflammation and pathology. | |
| Small Nucleolar RNA Host Gene 7SNHG7 | rna | 1 | — | — | SNHG7 regulates inflammatory pathways and myocardial remodeling relevant to acute coronary syndrome progression. | |
| SNHG18SNHG18 | rna | 1 | — | — | SNHG18 is a long non-coding RNA regulated by CAD variants in smooth muscle cells that influences plaque inflammation. | |
| SOCS3SOCS3 | protein | 1 | — | ◆ | SOCS3 is a negative regulator of inflammatory cytokine signaling, suppressing macrophage-driven plaque inflammation during acute MI. | |
| Soluble MHC Class I Chain-Related Protein AMICA | protein | 1 | — | — | sMICA is an early marker of stress-induced immune activation and endothelial shedding during acute myocardial injury and plaque inflammation. | |
| Specificity Protein 1SP1 | protein | 1 | — | — | SP1 transcriptional regulation of inflammatory and lipid-metabolism genes in atherosclerotic plaque cells. | |
| Sphinganine | metabolite | 1 | — | — | Sphinganine, a sphingoid base precursor, accumulates in response to environmental particulate matter and mediates oxidative inflammation driving atherosclerosis | |
| SPI-B transcription factorSPIB | gene | 1 | — | — | SPIB controls transcriptional programs of immune tolerance that suppress post-MI inflammatory injury. | |
| Succinate dehydrogenaseSDHA | protein | 1 | — | ◆ | Succinate dehydrogenase impairment elevates succinate levels, coupling mitochondrial dysfunction to pro-inflammatory innate immune activation in atherosclerotic | |
| Succinate receptor 1SUCNR1 | gene | 1 | — | ◆ | SUCNR1 activation by succinate released during ischemia-reperfusion promotes inflammatory signaling and cardiac damage. | |
| SULT1E1SULT1E1 | protein | 1 | — | ◆ | Sulfotransferase SULT1E1 regulates estrogen-dependent vascular inflammation and atherosclerotic plaque development. | |
| Superoxide anion | metabolite | 1 | — | — | Superoxide anion inactivates nitric oxide, impairing endothelial vasodilation and promoting inflammation and plaque destabilization. | |
| T-cell immunoglobulin and mucin-domain containing-3HAVCR2 | protein | 1 | — | ◆ | Immune tolerance receptor expressed on inflammatory cells; dysregulation promotes pathogenic immune response in atherosclerotic plaque. | |
| Tanshinone IIA | metabolite | 1 | — | — | Tanshinone IIA modulates macrophage function and reduces inflammatory injury in myocardial infarction. | |
| TBK1TBK1 | gene | 1 | — | ◆ | TBK1 mediates inflammatory signaling cascades that destabilize atherosclerotic plaques and contribute to myocardial injury. | |
| Terminal complement complex | complex | 1 | — | — | Terminal complement complex activation marks systemic inflammatory cascade and prothrombotic state in acute MI. | |
| TGFBR3TGFBR3 | gene | 1 | — | ◆ | TGF-β receptor 3 modulates plaque inflammation and fibrotic stability via TGF-β pathway signaling. | |
| THBS3THBS3 | gene | 1 | — | ◆ | THBS3 modulates inflammatory responses and matrix remodeling in atherosclerotic plaques. | |
| Thioredoxin-interacting proteinTXNIP | protein | 1 | — | ◆ | TXNIP activates the NLRP3 inflammasome to drive atherosclerotic plaque inflammation, destabilization and rupture-prone progression. | |
| TLR5TLR5 | gene | 1 | — | ◆ | TLR5 activation drives monocyte and endothelial inflammation, amplifying atherosclerotic plaque destabilization and thrombotic risk. | |
| Toll-Like Receptor 9TLR9 | protein | 1 | — | ◆ | TLR9 activation by plaque-derived DAMPs and microbial motifs drives monocyte/macrophage-mediated plaque inflammation. | |
| Transcription Factor 3TCF3 | gene | 1 | — | — | TCF3 is a transcriptional regulator differentially expressed in type 2 diabetes with CAD, affecting immune cell differentiation. | |
| Transglutaminase 2TGM2 | protein | 1 | — | ◆ | TGM2 drives plaque inflammation through cross-linking of inflammatory mediators and matrix proteins. | |
| Transient Receptor Potential Cation Channel Subfamily M Member 4TRPM4 | gene | 1 | — | ◆ | TRPM4 activation amplifies proinflammatory Ca2+ signaling in leukocytes and cardiomyocytes, exacerbating plaque inflammation and ischemic injury post-MI. | |
| Transmembrane Activator and Calcium-Modulator and Cyclophilin Ligand InteractorTNFRSF13B | protein | 1 | — | ◆ | TACI mediates B-cell activation and immunoglobulin production; altered TACI signaling affects adaptive immunity in plaque inflammation and correlates with myoca | |
| tRF-Gly-GCC-06 | rna | 1 | — | — | Small RNA fragment mobilizing macrophage-driven plaque inflammation in acute coronary syndrome. | |
| Tumor Necrosis Factor-Related Apoptosis-Inducing LigandTNFSF10 | protein | 1 | — | ◆ | TRAIL promotes apoptosis in plaque macrophages and contributes to ventricular remodeling; inverse LVEF correlation reflects cardiomyocyte loss and dysfunction. | |
| TWIST family bHLH transcription factor 1TWIST1 | gene | 1 | — | — | TWIST1 drives inflammatory and fibrotic remodeling in atherosclerotic arterial walls. | |
| UBR2UBR2 | gene | 1 | — | ◆ | UBR2 regulates protein quality control and inflammatory signaling in vascular disease. | |
| Vanin-1VNN1 | protein | 1 | — | ◆ | VNN1 enhances NF-κB signaling to amplify post-MI inflammation and cardiac remodeling. | |
| Vascular Adhesion Protein-1AOC3 | protein | 1 | — | ◆ | VAP-1 promotes leukocyte recruitment to inflamed endothelium and amplifies reperfusion injury in acute MI. | |
| ViperinVIPERIN | protein | 1 | — | — | Interferon-stimulated effector protein whose elevation in microvesicles reflects systemic antiviral and inflammatory immune activation. | |
| VLA-4ITGA4 | protein | 1 | — | ◆ | VLA-4 (α4β1 integrin) mediates monocyte adhesion to endothelial VCAM-1, promoting leukocyte recruitment and plaque destabilization. | |
| XXbac-B33L19.4 | rna | 1 | — | — | Circulating lncRNA regulating apoptosis and autophagy pathways implicated in atherosclerotic plaque destabilization and myocardial injury. | |
| Colony stimulating factor 3 receptorCSF3R | gene | — | — | ✦◆ | Regulates neutrophil recruitment and inflammatory cell activation in plaque inflammation. | |
| Nectin cell adhesion molecule 2NECTIN2 | gene | — | — | ✦◆ | Adhesion molecule mediating leukocyte-endothelial engagement; supports plaque inflammation. | |
| Oncostatin MOSM | protein | — | — | ✦◆ | OSM drives macrophage and smooth-muscle activation in atherosclerotic plaque; elevated in acute inflammation. | |
| PDGF-DPDGFDDN | gene | — | — | ✦ | Chemotactic growth factor promoting vascular inflammation and smooth-muscle-cell migration. |
Fibrous-cap degradation & rupture
Cap degradation / rupture79| Molecule | Type | Conf. | Refs | Trials | Evidence | Mechanism |
|---|---|---|---|---|---|---|
| Matrix metalloproteinase-9MMP9 | protein | 39 | — | ✦◆ | MMP-9 degrades extracellular matrix in the atherosclerotic fibrous cap, promoting rupture and thrombotic exposure. | |
| Matrix Metalloproteinase-2MMP2 | protein | 13 | — | ◆ | MMP-2 degrades the fibrous cap and myocardial ECM, mediating plaque rupture and post-infarction ventricular remodeling. | |
| Pregnancy-associated Plasma Protein APAPPA | protein | 11 | — | ✦◆ | PAPP-A is a metalloproteinase elevated in atherosclerotic plaques that degrades extracellular matrix, promoting cap rupture and thrombosis. | |
| Collagen Type I Alpha 1COL1A1 | protein | 10 | — | ◆ | COL1A1 is the major fibrous-cap structural protein; its exposure upon rupture initiates platelet adhesion and thrombosis. | |
| Tissue inhibitor of metalloproteinases-1TIMP1 | protein | 7 | — | ◆ | TIMP-1 inhibits MMP-driven fibrous-cap degradation and mediates ECM remodeling and cardiac fibrosis post-MI. | |
| Cathepsin DCTSD | protein | 6 | — | ◆ | Cathepsin D degrades extracellular-matrix proteins in atherosclerotic plaques and mediates macrophage apoptosis post-MI, influencing plaque stability and myocar | |
| Matrix metalloproteinase-3MMP3 | protein | 6 | — | ◆ | MMP-3 degrades fibrous-cap collagen and proteoglycans, promoting plaque destabilization and rupture. | |
| ADAMTS7 (A Disintegrin and Metalloproteinase with Thrombospondin Motifs 7)ADAMTS7 | gene | 5 | — | ◆ | Matrix metalloproteinase promoting fibrous-cap degradation, arterial calcification, and endothelial dysfunction driving atherosclerotic MI. | |
| LumicanLUM | protein | 4 | — | ◆ | Lumican cross-links collagen fibrils in the fibrous cap, reinforcing structural integrity against rupture. | |
| BiglycanBGN | protein | 3 | — | ◆ | Biglycan reinforces fibrous-cap ECM architecture and locally inhibits thrombin to protect plaque stability. | |
| Cathepsin LCTSL | protein | 3 | — | ◆ | Cathepsin L is a lysosomal cysteine protease that degrades atherosclerotic plaque extracellular matrix and also contributes to cardiomyocyte proteolysis during | |
| cathepsin SCTSS | protein | 3 | — | ◆ | Cathepsin S is a macrophage lysosomal protease that degrades fibrous-cap extracellular matrix in atherosclerosis. | |
| Collagen Type III Alpha 1 ChainCOL3A1 | protein | 3 | — | ◆ | COL3A1 is a structural collagen component of the fibrous cap; its remodeling/turnover marks plaque degradation and post-MI healing. | |
| Fibrinogen-Like Protein 1FGL1 | protein | 3 | — | ◆ | FGL1 is released following plaque rupture and participates in inflammatory and hemostatic responses, potentially stabilizing or propagating the thrombus. | |
| Matrix metalloproteinase-1MMP1 | protein | 3 | — | ✦◆ | Matrix metalloproteinase-1 degrades fibrous cap collagen and extracellular matrix, triggering atherosclerotic plaque rupture and thrombus exposure. | |
| Procollagen C-Endopeptidase EnhancerPCOLCE | protein | 3 | — | ◆ | PCOLCE promotes fibrous-cap collagen proteolysis and extracellular-matrix remodeling, facilitating plaque rupture and post-MI remodeling. | |
| proline | metabolite | 3 | — | — | Proline metabolism, a marker of collagen turnover, may discriminate plaque erosion from rupture mechanisms in Type 1 MI pathogenesis. | |
| VersicanVCAN | protein | 3 | — | ◆ | Versican remodeling in the fibrous cap reduces structural integrity and promotes cap degradation. | |
| α-Smooth Muscle ActinACTA2 | protein | 3 | — | — | ACTA2 (α-SMA) marks myofibroblast activation and fibrotic remodeling of the atherosclerotic plaque and myocardium. | |
| ADAMTS4ADAMTS4 | protein | 2 | — | ◆ | ADAMTS4 metalloprotease degrades versican and other proteoglycans in the atherosclerotic plaque extracellular matrix, promoting fibrous-cap thinning and remodel | |
| ALDH4A1ALDH4A1 | protein | 2 | — | ◆ | ALDH4A1 autoimmunity marks atherosclerotic plaque instability and fibrous-cap erosion. | |
| Cathepsin BCTSB | protein | 2 | — | ◆ | Cathepsin B degrades collagen and elastin in the fibrous cap, promoting thinning and rupture in unstable plaques. | |
| ChymaseCMA1 | protein | 2 | — | ✦◆ | Chymase from activated mast cells degrades fibrous-cap matrix proteins, contributing to cap thinning and rupture in destabilizing plaques. | |
| COL4A1COL4A1 | gene | 2 | — | ✦◆ | COL4A1 maintains plaque stability through collagen IV production and supports smooth-muscle-cell survival; its remodeling marks post-MI fibrosis. | |
| COL4A2COL4A2 | gene | 2 | — | ✦◆ | COL4A2 variants confer coronary artery disease susceptibility via effects on collagen IV-mediated plaque stabilization and fibrous-cap integrity. | |
| Collagen type I alpha-2 chainCOL1A2 | gene | 2 | — | ◆ | COL1A2 is the predominant fibrillar collagen dysregulated in post-MI fibrotic remodeling. | |
| Collagen VI alpha-3COL6A3 | gene | 2 | — | ✦◆ | COL6A3 maintains extracellular matrix integrity in the arterial wall and atherosclerotic plaque, supporting fibrous-cap resistance to degradation. | |
| Hyaluronic Acid | metabolite | 2 | — | — | Hyaluronic acid is an ECM regulator whose elevated plasma levels reflect matrix turnover during atherosclerotic plaque destabilization and erosion. | |
| Interferon-Inducible T-Cell Alpha ChemoattractantCXCL11 | protein | 2 | — | ◆ | I-TAC is elevated in ruptured atherosclerotic plaques, reflecting leukocyte recruitment and inflammatory destabilization of the fibrous cap. | |
| Matrix Metalloproteinase-12MMP12 | protein | 2 | — | ◆ | MMP-12 mediates extracellular matrix degradation and infarct remodeling in MI. | |
| Plasminogen Activator, UrokinasePLAU | gene | 2 | — | ✦◆ | PLAU encodes urokinase, a serine protease that degrades fibrin and extracellular matrix, contributing to fibrous-cap rupture and thrombus formation. | |
| Thrombospondin-4THBS4 | protein | 2 | — | ◆ | Thrombospondin-4 is an ECM protein dysregulated in atherosclerotic plaque progression and fibrous-cap remodeling. | |
| Tissue Inhibitor of Metalloproteinases 2TIMP2 | protein | 2 | — | ◆ | TIMP2 suppresses matrix metalloproteinase activity, protecting fibrous-cap collagen from degradation. | |
| ADAM9ADAM9 | protein | 1 | — | ◆ | ADAM9 proteolytic activity destabilizes the atherosclerotic plaque fibrous cap via matrix degradation, promoting rupture. | |
| ADAMTS1 (A Disintegrin and Metalloproteinase with Thrombospondin Motifs 1)ADAMTS1 | gene | 1 | — | ◆ | ADAMTS1 upregulation contributes to fibrous-cap degradation and atherosclerotic plaque rupture. | |
| Aggrecanase | protein | 1 | — | — | Aggrecanase-mediated degradation of plaque extracellular matrix reduces fibrous cap integrity and increases rupture risk. | |
| Alpha-1 AntitrypsinSERPINA1 | protein | 1 | — | ◆ | Alpha-1 antitrypsin inhibits neutrophil elastase and matrix metalloproteinases, protecting fibrous-cap integrity in atherosclerotic plaques. | |
| Amyloid-beta 1-40 | peptide | 1 | — | — | Amyloid-beta 1-40 destabilizes atherosclerotic plaques by promoting matrix degradation, precipitating rupture and thrombosis. | |
| Bone Morphogenetic Protein 1BMP1 | protein | 1 | — | ◆ | BMP1 regulates extracellular matrix remodeling and collagen degradation in atherosclerotic lesions. | |
| Calponin-2CNN2 | gene | 1 | — | ◆ | CNN2 dysregulation alters smooth-muscle cell function and plaque structural integrity. | |
| Cartilage oligomeric matrix proteinCOMP | protein | 1 | — | ◆ | COMP participates in fibrous-cap matrix degradation and tissue remodeling following myocardial injury. | |
| Cathepsin | protein | 1 | — | — | Cathepsin proteolysis of extracellular matrix proteins weakens the fibrous cap and promotes plaque rupture. | |
| Cathepsin ACTSA | protein | 1 | — | ◆ | CTSA (cathepsin A) degrades fibrous-cap matrix and contributes to plaque instability; targeting it may stabilize lesions post-MI. | |
| cathepsin KCTSK | protein | 1 | — | ◆ | Cathepsin K is a macrophage lysosomal protease elevated in atherosclerosis, contributing to fibrous-cap matrix degradation. | |
| Cathepsin XCTSX | protein | 1 | — | — | Cathepsin X, a macrophage-derived protease, degrades fibrous-cap collagen and elastin, promoting plaque rupture in acute coronary syndromes. | |
| CFDP1CFDP1 | gene | 1 | — | — | CFDP1 regulates smooth-muscle cell function and may contribute to fibrous-cap maintenance and stability. | |
| Collagen type V alpha-2 chainCOL5A2 | gene | 1 | — | ◆ | COL5A2 is a structural collagen involved in post-MI fibrotic cardiac remodeling. | |
| Collagen Type VI Alpha 1COL6A1 | gene | 1 | — | ◆ | COL6A1 is a fibrous-cap collagen subject to degradation during plaque rupture. | |
| Collagen VI Alpha-2 ChainCOL6A2 | protein | 1 | — | ◆ | COL6A2 expression and integrity in the plaque matrix reflect cap stability; reduced levels indicate erosion-prone remodeling. | |
| DecorinDCN | protein | 1 | — | ◆ | Decorin is a key ECM proteoglycan whose abundance and crosslinking state determine fibrous-cap mechanical integrity and rupture susceptibility. | |
| ElafinPI3 | protein | 1 | — | ◆ | Serine-protease inhibitor that counterbalances matrix degradation during plaque destabilization and rupture. | |
| Extracellular Matrix Protein 1ECM1 | protein | 1 | — | ◆ | ECM1 affects extracellular matrix integrity and vascular stability in SCAD. | |
| Fetuin-BFETUB | protein | 1 | — | ◆ | Fetuin-B modulates protease activity and extracellular matrix remodeling affecting fibrous-cap stability and rupture susceptibility. | |
| GPNMBGPNMB | protein | 1 | — | ◆ | GPNMB regulates inflammation and extracellular matrix deposition post-MI, influencing fibrous cap stability and plaque remodeling. | |
| GZMBGZMB | protein | 1 | — | ◆ | Granzyme B from infiltrating cytotoxic lymphocytes degrades fibrous-cap collagen and is a plaque vulnerability driver in Type 1 MI. | |
| Kallikrein-6KLK6 | protein | 1 | — | ◆ | Kallikrein protease contributes to matrix degradation and plaque instability preceding Type 1 MI. | |
| Laminin-1 (α1β1γ1)LAMA1 | protein | 1 | — | ◆ | Basement-membrane component marking severe myocardial necrosis and ventricular remodeling in extensive infarction. | |
| Latent TGF-Beta Binding Protein 1LTBP1 | protein | 1 | — | ◆ | LTBP1 sequesters latent TGF-β and stabilizes extracellular matrix, protecting the fibrous cap. | |
| LR11SORL1 | protein | 1 | — | ◆ | Lipoprotein-receptor family member regulating smooth-muscle proliferation and cap composition. | |
| MAP1SMAP1S | gene | 1 | — | — | MAP1S regulates smooth-muscle cell phenotype and may influence fibrous-cap stability in atherosclerosis. | |
| Matrix Metalloproteinase-25MMP25 | protein | 1 | — | ◆ | MMP-25 drives fibrous cap degradation and post-infarct ventricular remodeling. | |
| Matrix Metalloproteinase-7MMP7 | protein | 1 | — | ✦◆ | MMP-7 degrades fibrous-cap collagen and proteoglycans, promoting cap destabilization and rupture, and is elevated in CAD and MI patients. | |
| miR-221 | rna | 1 | — | — | miR-221 regulates vascular smooth-muscle proliferation and endothelial function relevant to plaque stability and stenosis severity. | |
| miR-222 | rna | 1 | — | — | miR-222 regulates vascular remodeling and endothelial function influencing plaque stability and coronary stenosis severity. | |
| miR-324-3p | rna | 1 | — | — | miR-324-3p is dysregulated in plaque rupture, potentially regulating extracellular-matrix remodeling. | |
| miR-379 | rna | 1 | — | — | miR-379 suppresses vascular smooth muscle cell proliferation, influencing fibrous-cap integrity and atherosclerotic plaque stability. | |
| miR-744-3p | rna | 1 | — | — | miR-744-3p is dysregulated in plaque rupture, potentially modulating matrix-degradation or inflammatory pathways. | |
| NidogenNID1 | protein | 1 | — | ◆ | Nidogen maintains basement-membrane structure supporting fibrous-cap stability and endothelial barrier function. | |
| Proteinase 3PRTN3 | protein | 1 | — | ◆ | Proteinase 3 released by activated neutrophils degrades fibrous-cap matrix proteins, promoting cap thinning and rupture. | |
| Proteoglycan 4PRG4 | protein | 1 | — | ◆ | Proteoglycan 4 contributes to extracellular matrix organization and plaque structural stability. | |
| PRSS23PRSS23 | protein | 1 | — | ◆ | PRSS23 is a trypsin-like serine protease; smoking-associated variants may affect fibrous-cap matrix turnover in AMI. | |
| RAB39ARAB39A | protein | 1 | — | ◆ | RAB39A dysregulation associates with atherosclerotic plaque rupture and acute coronary events in Type 1 MI. | |
| SPARC-Like Protein 1SPARCL1 | protein | 1 | — | ◆ | SPARCL1 maintains vessel wall structural integrity; its dysregulation compromises fibrous-cap stability in Type 1 MI. | |
| Thrombospondin Type 1 Domain Containing 4THSD4 | gene | 1 | — | ◆ | THSD4 supports structural integrity of connective tissue and aortic wall, reducing plaque rupture risk. | |
| TIMP metalloproteinase inhibitor 3TIMP3 | protein | 1 | — | ◆ | TIMP3 inhibition of matrix metalloproteinases protects fibrous-cap integrity, preventing plaque rupture and thrombotic occlusion. | |
| Tissue Inhibitor of Metalloproteinases-4TIMP4 | protein | 1 | — | ◆ | TIMP4 inhibits matrix metalloproteinase activity, protecting the fibrous cap from degradation and rupture. | |
| Transforming Growth Factor Beta Receptor IITGFBR2 | gene | 1 | — | ◆ | TGFBR2 mediates TGF-β signaling controlling smooth-muscle proliferation and extracellular-matrix remodeling during fibrous-cap thinning. | |
| Trypsin | protein | 1 | — | — | Trypsin degrades fibrous-cap collagen and elastin while activating protease-activated receptors that destabilize the plaque. | |
| Heat shock protein 47 (HSP47)SERPINH1 | gene | — | — | ✦◆ | Stabilizes and matures interstitial collagen in plaque fibrous cap, reducing rupture risk. |
Endothelial activation & erosion
Endothelial activation/erosion135| Molecule | Type | Conf. | Refs | Trials | Evidence | Mechanism |
|---|---|---|---|---|---|---|
| von Willebrand factorVWF | protein | 60 | — | ◆ | vWF exposure following endothelial activation enables platelet adhesion and thrombotic cascade initiation. | |
| sVCAM-1VCAM1 | protein | 44 | — | ◆ | Soluble VCAM-1 is an endothelial adhesion molecule upregulated during endothelial activation and dysfunction; it mediates leukocyte recruitment into atheroscler | |
| Intercellular Adhesion Molecule 1ICAM1 | protein | 43 | — | ◆ | sICAM-1 reflects endothelial activation and leukocyte recruitment to atherosclerotic plaques and coronary injury sites. | |
| E-selectinSELE | protein | 30 | — | ◆ | E-selectin expression on endothelium marks activation and enables leukocyte rolling and adhesion during plaque inflammation and erosion. | |
| thrombomodulinTHBD | protein | 23 | — | ◆ | Thrombomodulin shedding from damaged endothelium impairs anticoagulation and indicates endothelial erosion/dysfunction in acute coronary events. | |
| Nitric oxide | metabolite | 22 | 3 | — | Nitric oxide produced by endothelial cells regulates vasodilation and suppresses platelet adhesion; reduced bioavailability reflects endothelial dysfunction and | |
| Endothelial nitric oxide synthaseNOS3 | protein | 22 | — | ✦◆ | Endothelial NOS catalyzes NO production essential for vasodilation and platelet inhibition; dysfunction contributes to endothelial erosion and thrombosis. | |
| Vascular endothelial growth factorVEGFA | protein | 20 | 1 | ◆ | VEGF promotes endothelial repair, angiogenesis and endothelial progenitor cell mobilization following myocardial injury and revascularization therapy. | |
| CD31 | protein | 19 | — | — | CD31 marks endothelial cell activation and erosion in sEVs, indicating endothelial dysfunction and superficial erosion in Type 1 MI pathology. | |
| homocysteine | metabolite | 17 | — | — | Elevated homocysteine impairs endothelial function and promotes oxidative modification of LDL, accelerating atherosclerotic lipid retention and plaque vulnerabi | |
| PECAM-1PECAM1 | protein | 14 | — | ✦◆ | PECAM-1 mediates endothelial cell–cell and endothelial–platelet adhesion; dysfunction reflects endothelial activation and increased thrombotic risk. | |
| CD34 | protein | 12 | — | — | Circulating CD34+ endothelial progenitor and endothelial cells mark endothelial erosion and reparative responses in MI. | |
| Soluble lectin-like oxidized LDL receptor 1OLR1 | protein | 11 | 1 | ✦◆ | Soluble LOX-1 reflects endothelial activation, oxidized-lipoprotein uptake, and pro-thrombotic endothelial dysfunction in acute coronary syndrome and Type 1 MI. | |
| Vascular Endothelial CadherinCDH5 | protein | 11 | — | ◆ | Vascular endothelial cadherin cleavage destabilizes endothelial junctions, enabling transmigration and exposing subendothelial matrix. | |
| Thrombospondin-1THBS1 | protein | 9 | — | ◆ | Thrombospondin-1 mediates endothelial erosion and platelet-leukocyte engagement, modulating thrombus formation and post-MI inflammation. | |
| VEGFR-2 (KDR)KDR | protein | 9 | — | ◆ | VEGFR-2 on circulating endothelial cells and EPCs marks endothelial activation, injury and angiogenic response in Type 1 MI. | |
| Endothelin-1EDN1 | peptide | 8 | 1 | ◆ | ET-1 drives endothelial activation, excessive vasoconstriction, and endocardial injury during acute MI, with predictive value for endothelial progenitor cell mo | |
| Asymmetric dimethylarginine | metabolite | 7 | 2 | — | ADMA inhibits endothelial NO synthase, impairing vasodilation and promoting endothelial dysfunction driving erosion. | |
| EndocanESM1 | protein | 6 | — | ◆ | Endocan marks endothelial activation, dysfunction and erosion that expose thrombogenic subendothelial surfaces in Type 1 MI. | |
| Prostacyclin | metabolite | 6 | — | — | Prostacyclin maintains endothelial function and opposes platelet activation, protecting against thrombosis in Type 1 MI. | |
| Angiotensin-Converting EnzymeACE | protein | 5 | 1 | ✦◆ | ACE generates angiotensin II, promoting endothelial dysfunction, vascular inflammation, and pro-thrombotic state in coronary atherosclerosis. | |
| Angiotensin II | peptide | 5 | — | — | Angiotensin II drives endothelial activation, impairs vasodilation, and amplifies plaque inflammation via LOX-1 and NADPH-oxidase signaling. | |
| arginine | metabolite | 5 | — | — | Arginine dysregulation impairs endothelial NO synthesis, reducing vasodilation and promoting endothelial dysfunction while delaying myocardial recovery from isc | |
| CD146 | protein | 5 | — | — | Soluble CD146 and circulating CD146+ endothelial cells and microparticles mark endothelial injury, erosion, and post-MI angiogenesis. | |
| Endothelial protein C receptorPROCR | gene | 5 | — | ✦◆ | PROCR encodes the endothelial protein C receptor, an antithrombotic and anti-inflammatory regulator whose expression is altered during endothelial dysfunction a | |
| FMS-Like Tyrosine Kinase 1FLT1 | gene | 5 | — | ✦◆ | FLT1 dysfunction impairs endothelial homeostasis and is associated with coronary artery disease and myocardial infarction risk. | |
| HIF1AHIF1A | gene | 5 | — | ◆ | HIF1A-driven endothelial-mesenchymal transition, mitochondrial dysfunction and reduced cardioprotective secretome promote endothelial erosion and myocardial inj | |
| Phosphatase and actin regulator 1PHACTR1 | gene | 5 | — | ✦◆ | Phosphatase regulating actin dynamics in endothelial dysfunction, arterial calcification, and fibrous-cap degradation driving plaque vulnerability and rupture. | |
| Noradrenaline | metabolite | 4 | 1 | — | Noradrenaline promotes endothelial activation and dysfunction, increases platelet reactivity, and alters thrombus architecture in atherothrombotic MI. | |
| ADAMTS13ADAMTS13 | protein | 4 | — | ◆ | ADAMTS13 deficiency permits ultralarge VWF multimer accumulation, amplifying platelet adhesion and thrombotic risk in acute coronary events. | |
| Angiopoietin-2ANGPT2 | protein | 4 | — | ◆ | Angiopoietin-2 promotes endothelial activation and vascular instability, destabilizing the coronary endothelium and exacerbating post-MI remodeling. | |
| EndoglinENG | protein | 4 | — | ◆ | Endoglin regulates endothelial function and vascular remodeling; elevated levels reflect endothelial activation and plaque neoangiogenesis associated with ather | |
| NOS1NOS1 | gene | 4 | — | ✦◆ | NOS1 dysregulation impairs nitric oxide production, promoting endothelial dysfunction and macrophage-endothelial interactions in atherosclerosis. | |
| Nuclear factor erythroid 2-related factor 2NFE2L2 | protein | 4 | — | ◆ | Nrf2 activates endothelial protective antioxidant responses and suppresses dysfunction-driven cap erosion. | |
| Syndecan-1SDC1 | protein | 4 | — | ◆ | Syndecan-1 shedding from damaged endothelium marks endothelial activation and erosion-driven Type 1 MI pathogenesis. | |
| Endothelin | protein | 3 | 1 | — | Endothelin-1 mediates endothelial dysfunction and excessive vasoconstriction during acute coronary events, contributing to reduced coronary blood flow and myoca | |
| Angiotensin-Converting Enzyme 2ACE2 | protein | 3 | — | ◆ | ACE2 elevation in acute MI reflects endothelial activation and dysfunction; modulates angiotensin signaling and inflammatory responses in the coronary vasculatu | |
| Epidermal Growth FactorEGF | protein | 3 | — | ◆ | EGF acts as a marker of endothelial erosion and tissue injury in acute coronary syndromes, correlating with ischemic time and extent of myocardial damage. | |
| ERG (ETS-related gene)ERG | gene | 3 | — | ◆ | ETS transcription factor regulates endothelial phenotype and is dysregulated in STEMI, also involved in platelet immunoglobulin responses. | |
| FoxO1FOXO1 | gene | 3 | — | ◆ | FoxO1 transcription-factor dysregulation in coronary artery disease impairs endothelial function and promotes atherosclerotic vascular remodeling. | |
| Interleukin-16IL16 | protein | 3 | — | ◆ | IL-16 promotes T-cell and eosinophil recruitment and contributes to endothelial activation, erosion, and inflammatory remodeling in acute coronary syndromes. | |
| Pigment epithelium-derived factorSERPINF1 | protein | 3 | — | ◆ | PEDF is an anti-inflammatory and atheroprotective factor that prevents endothelial dysfunction and atherosclerotic plaque destabilization. | |
| VitronectinVTN | protein | 3 | — | ◆ | Vitronectin is an adhesive glycoprotein mediating endothelial dysfunction and platelet adhesion in atherothrombotic injury. | |
| β-CateninCTNNB1 | protein | 3 | — | ◆ | CTNNB1 promotes endothelial dysfunction and vascular remodeling via EndMT pathways. | |
| TryptaseTPSAB1 | protein | 2 | 1 | ◆ | Tryptase is a mast cell-derived serine protease that degrades endothelial extracellular matrix and contributes to endothelial erosion in Type 1 MI. | |
| Bone Morphogenetic Protein 4BMP4 | protein | 2 | — | ◆ | BMP-4 promotes endothelial dysfunction and vascular inflammation, contributing to plaque destabilization and progression toward rupture or erosion. | |
| Citrulline | metabolite | 2 | — | — | Citrulline reflects arginine bioavailability and nitric oxide synthesis, modulating endothelial activation and vasomotor function. | |
| Endothelial microparticles | complex | 2 | — | — | Microparticles shed from activated/eroded endothelium reflecting endothelial damage and thrombotic potential. | |
| Insulin-like Growth Factor-1IGF1 | protein | 2 | — | ◆ | IGF1 promotes endothelial survival and ECM remodeling, contributing to plaque stability and reduced erosion risk. | |
| Integrin Alpha-VITGAV | protein | 2 | — | ✦◆ | CD51+ endothelial microparticles circulate during acute MI, reflecting endothelial cell activation, injury, and shedding of membrane fragments during coronary t | |
| Jagged1JAG1 | protein | 2 | — | ◆ | Jagged1 participates in Notch signaling controlling endothelial activation and angiogenesis, modulating vascular inflammation and remodeling in Type 1 MI. | |
| JCADJCAD | gene | 2 | — | ✦ | JCAD directly drives endothelial dysfunction and atherosclerotic plaque formation, contributing to Type 1 MI risk through endothelial erosion and CAD. | |
| Krüppel-like Factor 2KLF2 | gene | 2 | — | — | KLF2 downregulation impairs endothelial shear-stress sensing and homeostasis, promoting endothelial erosion and Type 1 MI. | |
| L-arginine | metabolite | 2 | — | — | L-arginine availability limits nitric oxide production, and its depletion associates with endothelial dysfunction and ACS severity. | |
| microRNA-145MIR145 | rna | 2 | — | — | miR-145 dysregulation promotes endothelial dysfunction during plaque evolution and predicts post-MI adverse outcomes. | |
| miR-126-3p | rna | 2 | — | — | miR-126-3p regulates vascular endothelial tight junctions and angiogenic signaling, serving as a circulating biomarker for endothelial activation and CAD/MI ris | |
| miR-330-3p | rna | 2 | — | — | miRNA suppressing RGS5-mediated endothelial stability, facilitating rupture-prone plaque development. | |
| NADPH oxidaseNOX2 | protein | 2 | — | — | NADPH oxidase generates superoxide driving lipid oxidation and endothelial dysfunction, destabilizing plaques. | |
| NOTCH1NOTCH1 | gene | 2 | — | ◆ | NOTCH1 signaling controls endothelial biology and vascular calcification, contributing to plaque stability and coronary thrombosis risk. | |
| PerlecanHSPG2 | protein | 2 | — | ◆ | HSPG2 upregulation in CAD reflects endothelial remodeling and matrix turnover destabilizing the fibrous cap. | |
| RGS5RGS5 | protein | 2 | — | ◆ | G-protein regulator maintaining endothelial barrier function; miR-330-3p-suppressed in MI progression. | |
| Scavenger receptor class B member 1SCARB1 | protein | 2 | — | ✦◆ | SCARB1 mediates endothelial uptake of HDL and cardioprotective signals regulating plaque inflammation. | |
| Soluble amyloid precursor protein 770 | peptide | 2 | — | — | sAPP770 is released from activated endothelium during acute coronary syndromes, reflecting endothelial injury and dysfunction. | |
| Symmetric dimethylarginine | metabolite | 2 | — | — | Symmetric dimethylarginine inhibits nitric-oxide synthase, promoting endothelial dysfunction and erosion. | |
| Urotensin II | peptide | 2 | — | — | Urotensin II promotes vasoconstriction and endothelial activation, contributing to coronary atherosclerotic disease. | |
| Neuregulin-1NRG1 | protein | 1 | 1 | ◆ | Neuregulin-1 activates ERBB2/ERBB4 signaling in endothelial cells, suppressing endothelial-to-mesenchymal transition and stabilizing vascular integrity. | |
| 15(S)-HETE | metabolite | 1 | — | — | 15(S)-HETE is an eicosanoid that impairs endothelial function and promotes vascular inflammation. | |
| Actin Filament Associated Protein 1AFAP1 | protein | 1 | — | — | AFAP1 regulates cytoskeletal dynamics and vascular integrity in SCAD. | |
| Amyloid Precursor Protein isoform 770APP | protein | 1 | — | ◆ | APP770 regulates endothelial cell viability and vascular inflammation, contributing to atherosclerotic plaque instability. | |
| ANGPTL6ANGPTL6 | protein | 1 | — | ◆ | ANGPTL6 promotes endothelial repair and stent endothelialization to restore coronary integrity. | |
| ARVCFARVCF | gene | 1 | — | ◆ | ARVCF is a CAD-variant-regulated adherens-junction protein that influences endothelial integrity and vascular inflammation. | |
| ATPase plasma membrane Ca2+ ATPase 1ATP2B1 | gene | 1 | — | ✦◆ | Plasma-membrane calcium pump maintaining intracellular calcium homeostasis in vascular smooth muscle and endothelium, influencing vascular tone and reactivity. | |
| Cadherin-15CDH15 | protein | 1 | — | ◆ | CDH15 dysregulation compromises endothelial integrity and promotes leukocyte recruitment in acute MI. | |
| CD148PTPRJ | protein | 1 | — | ◆ | CD148 is a vascular receptor phosphatase that regulates endothelial adhesion and barrier function, modulating plaque erosion. | |
| Coxsackievirus and Adenovirus ReceptorCXADR | gene | 1 | — | ◆ | CXADR variants confer CAD susceptibility through altered endothelial adhesion molecule expression and leukocyte interaction. | |
| CPEB1CPEB1 | gene | 1 | — | — | CPEB1 controls endothelial cell apoptosis and inflammatory pathways contributing to endothelial erosion. | |
| Desmocollin-1DSC1 | protein | 1 | — | ◆ | DSC1 maintains endothelial integrity; loss promotes vascular inflammation and plaque progression. | |
| DHX38DHX38 | gene | 1 | — | ◆ | DHX38 regulates vascular endothelial cell senescence, contributing to endothelial activation and erosion in coronary atherothrombosis. | |
| Endothelial and Smooth Muscle Protein-1C5ORF46 | protein | 1 | — | ◆ | EMPRINN elevation in epicardial adipose tissue during NSTEMI reflects adipose inflammation and endothelial dysfunction in coronary vasculature. | |
| Endothelial Cell Selective Adhesion MoleculeESAM | protein | 1 | — | ◆ | ESAM is an endothelial-cell adhesion molecule marking activation and integrity loss after coronary intervention. | |
| EpiregulinEREG | protein | 1 | — | ◆ | EREG promotes endothelial repair and angiogenic remodeling to restore coronary perfusion after MI. | |
| Epoxyeicosatrienoic Acid | metabolite | 1 | — | — | Epoxyeicosatrienoic acid promotes endothelial function and vasodilation, suppressing inflammatory pathways implicated in plaque erosion and instability. | |
| ERK5MAPK7 | protein | 1 | — | ◆ | ERK5 mediates endothelial-cell homeostasis and prevents dysfunction-driven erosion and thrombosis. | |
| Fibroblast growth factor receptor 1FGFR1 | protein | 1 | — | ◆ | FGFR1 mediates fibroblast growth factor signaling in endothelial cells, influencing plaque vascularization, inflammation, and atherothrombotic vulnerability. | |
| Forkhead box M1FOXM1 | gene | 1 | — | ◆ | FOXM1 transcriptional activation promotes endothelial-to-mesenchymal transition, reducing endothelial integrity and contributing to vascular dysfunction in athe | |
| Four and a half LIM domains 5FHL5 | gene | 1 | — | ✦ | LIM-domain protein regulating vascular remodeling and calcification that influences atherosclerotic plaque stability and cap integrity. | |
| Granulocyte colony-stimulating factorCSF3 | protein | 1 | — | ✦◆ | G-CSF improves endothelial function and mobilizes bone-marrow-derived progenitors contributing to vascular repair after myocardial infarction. | |
| GUCY1A1GUCY1A1 | gene | 1 | — | ✦◆ | GUCY1A1 CAD-associated variants impair nitric-oxide signaling in the endothelium, promoting dysfunction and atherothrombotic risk. | |
| Hes Family BHLH Transcription Factor 1HES1 | gene | 1 | — | — | HES1 dysregulation impairs endothelial function and homeostasis, promoting vascular dysfunction and plaque progression. | |
| Intercellular Adhesion Molecule-2ICAM2 | protein | 1 | — | ◆ | ICAM-2 mediates endothelial-leukocyte interactions, promoting inflammatory cell infiltration in atherosclerotic lesions. | |
| LDL receptor-related protein 1LRP1 | gene | 1 | — | ◆ | Lipoprotein receptor and calcium regulator governing intracellular calcium homeostasis and endothelial function in atherosclerotic vasculature. | |
| LIM domain and actin-binding protein 1LIMA1 | gene | 1 | — | ◆ | Actin-binding protein regulating cytoskeletal dynamics in vascular contraction and endothelial barrier integrity. | |
| Melanoma Cell Adhesion MoleculeMCAM | protein | 1 | — | ◆ | MCAM mediates leukocyte adhesion and endothelial activation, contributing to vascular inflammation during acute MI. | |
| microRNA-32-5p | rna | 1 | — | — | miR-32-5p impairs endothelial KLF2 expression, compromising endothelial mechanotransduction and promoting erosion-type MI. | |
| miR-103a | rna | 1 | — | — | miR-103a promotes endothelial dysfunction and serves as a biomarker for acute coronary events. | |
| miR-126-5p | rna | 1 | — | — | miR-126-5p regulates endothelial function and vascular integrity; its dysregulation associates with coronary artery disease. | |
| miR-139-5p | rna | 1 | — | — | miR-139-5p regulates vascular performance and endothelial function in coronary pathology. | |
| miR-199a-5p | rna | 1 | — | — | miR-199a-5p regulates vascular performance and endothelial function in coronary pathology. | |
| miR-26a-5p | rna | 1 | — | — | miR-26a-5p regulates vascular performance and endothelial function in coronary pathology. | |
| miR-30b-5p | rna | 1 | — | — | miR-30b-5p regulates vascular performance and endothelial function in coronary pathology. | |
| miR-3667-3p | rna | 1 | — | — | miR-3667-3p differentially marks the endothelial erosion phenotype in Type 1 MI, distinguishing erosion-mediated acute coronary thrombosis from plaque rupture. | |
| miR-377 | rna | 1 | — | — | miR-377 is dysregulated during acute MI, modulating endothelial function and injury responses; elevated levels mark endothelial damage and dysfunction. | |
| miR-92a-3p | rna | 1 | — | — | miR-92a-3p, packaged in extracellular microvesicles, regulates angiogenesis and endothelial vascular stability in acute coronary syndromes. | |
| miR-let-7d-5p | rna | 1 | — | — | miR-let-7d-5p regulates vascular performance and endothelial function in coronary pathology. | |
| Nitrite | metabolite | 1 | — | — | Elevated nitrite indicates reactive oxygen species-driven oxidation of nitric oxide and impaired endothelial-protective NO signaling. | |
| Notch Receptor 3NOTCH3 | protein | 1 | — | ◆ | NOTCH3 signaling dysregulation impairs endothelial function and vascular homeostasis, promoting plaque inflammation. | |
| Oxidative stress responsive gene 1OSGIN1 | gene | 1 | — | — | OSGIN1 upregulation marks endothelial cell dysfunction and activation in plaque erosion-prone sites. | |
| Oxidative stress responsive gene 2OSGIN2 | gene | 1 | — | — | OSGIN2 upregulation indicates endothelial dysfunction and oxidative stress in plaque erosion-prone lesions. | |
| p27KIP1CDKN1B | protein | 1 | — | ◆ | A cyclin-dependent kinase inhibitor regulating vascular smooth muscle cell proliferation and atherosclerotic plaque remodeling. | |
| Phosphodiesterase 5PDE5A | protein | 1 | — | ◆ | PDE5 catalyzes cGMP hydrolysis; its inhibition preserves endothelial nitric-oxide signaling, reducing endothelial dysfunction and activation during atherosclero | |
| Piezo1PIEZO1 | protein | 1 | — | ◆ | Piezo1 senses mechanical stress on endothelial cells, modulating dysfunction in atherosclerotic disease. | |
| PIM3PIM3 | gene | 1 | — | ◆ | PIM3 kinase promotes endothelial dysfunction and vascular inflammation, contributing to atherosclerotic plaque destabilization and coronary thrombosis. | |
| PLPP3PLPP3 | protein | 1 | — | ✦◆ | PLPP3 regulates lysophospholipid signaling and endothelial quiescence; critical for hemodynamic mechanosensing and endothelial stability. | |
| Protein tyrosine kinase 7PTK7 | protein | 1 | — | ◆ | PTK7 dysregulation associates with endothelial dysfunction and vascular inflammation contributing to coronary atherosclerotic disease. | |
| Receptor tyrosine-protein kinase erbB-2ERBB2 | gene | 1 | — | ◆ | ERBB2, activated by neuregulin-1, transduces anti-inflammatory and anti-EndMT signals in endothelial cells, preserving barrier function and vascular stability. | |
| Receptor tyrosine-protein kinase erbB-4ERBB4 | gene | 1 | — | ◆ | ERBB4, activated by neuregulin-1, suppresses endothelial-to-mesenchymal transition and promotes endothelial cell survival during vascular injury and atheroscler | |
| RGM domain family member BRGMB | protein | 1 | — | ◆ | RGMB dysregulation associates with endothelial dysfunction and vascular remodeling in coronary artery disease. | |
| Secreted Frizzled-related protein 3SFRP3 | protein | 1 | — | — | sFRP3 antagonizes canonical Wnt signaling, suppressing endothelial-to-mesenchymal transition and maintaining endothelial barrier function during vascular injury | |
| Snail family transcriptional repressor 1SNAI1 | gene | 1 | — | ◆ | SNAIL transcriptional repressor drives endothelial-to-mesenchymal transition, reducing endothelial-cell adhesion and increasing vascular permeability in atheros | |
| soluble Fms-like Tyrosine Kinase-1 | protein | 1 | — | — | sFlt1 impairs endothelial function and angiogenesis, linking preeclampsia-like vascular pathology to atherosclerotic progression. | |
| Solute carrier family 24 member 3SLC24A3 | gene | 1 | — | ◆ | Calcium/sodium exchanger regulating intracellular calcium in vascular smooth muscle and endothelium, governing vascular reactivity and calcification. | |
| Sphingomyelin (42:3) | lipid | 1 | — | — | Sphingomyelin (42:3) protects endothelial cell integrity and reduces apoptosis, opposing erosion mechanisms. | |
| TAZWWTR1 | protein | 1 | — | ◆ | TAZ, activated downstream of JCAD, promotes endothelial dysfunction and contributes to atherosclerotic plaque instability. | |
| Trefoil Factor 3TFF3 | protein | 1 | — | ◆ | TFF3 promotes endothelial cell survival and angiogenic remodeling in the post-MI cardiac microenvironment. | |
| TRIOBPTRIOBP | protein | 1 | — | — | TRIOBP interacts with JCAD to stabilize endothelial stress fibers, preserving or modulating endothelial barrier integrity during atherosclerosis progression. | |
| Tyrosine-Protein Kinase Receptor TIE-2TEK | protein | 1 | — | ◆ | Tie-2 receptor maintains endothelial barrier integrity and angiogenic homeostasis; dysregulation promotes atherosclerotic erosion. | |
| Urotensin II Receptor | protein | 1 | — | — | Urotensin II receptor transduces vasoconstrictor and pro-inflammatory signals during atherosclerotic plaque evolution. | |
| YAPYAP1 | protein | 1 | — | ◆ | YAP, activated downstream of JCAD, promotes endothelial dysfunction and contributes to atherosclerotic plaque instability. | |
| Adhesion G Protein-Coupled Receptor L3ADGRL3 | gene | — | — | ✦◆ | Cell-adhesion receptor expressed on endothelium; plausible role in endothelial activation. | |
| Laminin subunit beta 2LAMB2 | gene | — | — | ✦◆ | LAMB2 maintains vascular basement-membrane structure; mutations cause endothelial erosion and alter plaque stability. | |
| Membrane-associated ring-CH-type finger 1MARCHF1 | gene | — | — | ✦◆ | Ubiquitin ligase regulating endothelial and immune cell protein homeostasis with unclear MI specificity. | |
| Muscle-associated Ras suppressorMRAS | gene | — | — | ✦◆ | Suppresses Ras signaling; loss linked to endothelial dysfunction and inflammatory activation. | |
| Protein tyrosine phosphatase non-receptor type 11PTPN11 | gene | — | — | ✦◆ | Regulates endothelial permeability and platelet activation via phosphatase signaling. | |
| Secreted Frizzled-Related Protein 1SFRP1 | gene | — | — | ✦◆ | SFRP1 suppresses Wnt signaling; loss promotes endothelial dysfunction, vascular calcification, and plaque inflammation. | |
| Tensin 1TNS1 | gene | — | — | ✦◆ | Modulates endothelial cell–cell junctions and integrin signaling affecting vascular integrity. |
Platelet adhesion & activation
Platelet activation231| Molecule | Type | Conf. | Refs | Trials | Evidence | Mechanism |
|---|---|---|---|---|---|---|
| P-selectinSELP | protein | 60 | — | ✦◆ | P-selectin mediates platelet activation and adhesion to endothelium, driving thrombotic cascade in MI. | |
| Soluble CD40 ligandCD40LG | protein | 59 | — | ✦◆ | sCD40L released from activated platelets amplifies endothelial dysfunction and platelet–leukocyte thrombotic crosstalk. | |
| Platelet Factor 4PF4 | protein | 32 | — | ◆ | PF4 is released upon platelet activation and serves as an early biomarker of platelet recruitment and thrombus formation in Type 1 MI. | |
| Beta-ThromboglobulinPPBP | protein | 25 | — | ◆ | Beta-thromboglobulin is released upon platelet activation and serves as an early AMI biomarker of platelet recruitment. | |
| Integrin alpha IIbITGA2B | protein | 25 | — | ✦◆ | ITGA2B-encoded integrin αIIb subunit forms the αIIbβ3 receptor essential for platelet aggregation and coronary thrombus formation in Type 1 MI. | |
| Glycoprotein VIGP6 | protein | 20 | — | ✦◆ | GPVI binds exposed collagen upon cap rupture or erosion, triggering platelet adhesion, activation, and thrombus propagation. | |
| Glycoprotein IbGP1BA | protein | 18 | — | ◆ | GPIb mediates platelet tethering to exposed von Willebrand factor at the site of endothelial rupture or erosion, initiating platelet adhesion and activation. | |
| Phosphatidylserine | lipid | 14 | — | — | Phosphatidylserine exposure on activated platelets and microparticles promotes platelet aggregation and thrombin generation. | |
| CD36 moleculeCD36 | protein | 13 | — | ◆ | CD36 acts as a platelet scavenger receptor for oxidized LDL, amplifying platelet activation and microvesicle formation during acute thrombosis. | |
| CD39ENTPD1 | protein | 13 | — | ◆ | CD39 ectonucleotidase hydrolyzes ATP and ADP to adenosine monophosphate, attenuating platelet activation and arterial thrombosis. | |
| FibronectinFN1 | protein | 12 | — | ✦◆ | Fibronectin mediates platelet adhesion to exposed matrix and fibroblast paracrine signaling; dysregulation marks plaque instability and thrombotic coronary even | |
| Adenosine diphosphate | metabolite | 11 | 1 | — | ADP released from platelet dense granules activates P2Y receptors, sustaining platelet aggregation and thrombus propagation. | |
| Integrin αIIbβ3 | protein | 11 | — | — | Integrin αIIbβ3 bridges platelets via fibrinogen binding, essential for platelet-dependent thrombus formation. | |
| phosphatidylethanolamine | lipid | 11 | — | — | Phosphatidylethanolamine dysregulation in platelets and monocytes contributes to platelet dysfunction and pro-thrombotic extracellular vesicle release in Type 1 | |
| ATP | metabolite | 8 | 1 | — | ATP depletion and extracellular accumulation drives platelet activation and signals myocardial ischemia during acute coronary occlusion. | |
| C-X-C Chemokine Receptor Type 4CXCR4 | gene | 8 | — | ✦◆ | CXCR4 mediates CXCL12-driven platelet activation and pro-thrombotic signaling, contributing to atherothrombotic cascade. | |
| CD11bITGAM | protein | 8 | — | ◆ | CD11b-mediated leukocyte activation and recruitment promote atherothrombotic plaque inflammation. | |
| Integrin β3ITGB3 | gene | 8 | — | ✦◆ | ITGB3 gene product (integrin β3) forms the fibrinogen receptor αIIbβ3, essential for platelet-platelet adhesion and thrombus consolidation. | |
| Protein kinase BAKT1 | gene | 8 | — | ◆ | AKT phosphorylation amplifies platelet activation via PI3K, while also promoting endothelial repair and cardiomyocyte survival through eNOS and mitochondrial pr | |
| P2Y12 ReceptorP2RY12 | gene | 7 | 5 | ✦◆ | P2Y12 is the platelet ADP receptor central to platelet aggregation and thrombosis; therapeutic target for antiplatelet therapy. | |
| CD63 moleculeCD63 | protein | 7 | — | ◆ | CD63 exposure on platelet extracellular vesicles indicates granule secretion and platelet activation during thrombus formation. | |
| adenosine | metabolite | 6 | 2 | — | Adenosine inhibits platelet activation and thrombus formation while promoting endothelial function and myocardial cardioprotection via ticagrelor-independent me | |
| Growth arrest-specific 6 (Gas6)GAS6 | protein | 6 | — | ◆ | Growth arrest-specific 6 is a vitamin-K-dependent ligand of the TAM receptor family (AXL, MERTK, TYRO3). Released on platelet activation, it signals through platelet TAM receptors to potentiate degranulation, integrin αIIbβ3 activation and clot stabilization, linking platelet activation to thrombus growth in atherothrombotic MI. The Gas6/AXL axis is also upregulated in STEMI and implicated in vascular inflammation. | |
| Neutrophil elastaseELANE | protein | 6 | — | ✦◆ | Neutrophil elastase activates both coagulation and platelet pathways, augmenting thrombus formation. | |
| P-selectin glycoprotein ligand-1SELPLG | protein | 6 | — | ◆ | PSGL-1 engages P-selectin on activated platelets, driving platelet-leukocyte crosstalk and prothrombotic amplification at the site of plaque rupture. | |
| TNF receptor 1TNFRSF1A | protein | 6 | — | ◆ | Soluble TNF receptor 1 promotes platelet activation and correlates with thrombotic tendency at the site of plaque rupture. | |
| CD73NT5E | protein | 5 | — | ◆ | CD73 5'-nucleotidase converts AMP to adenosine, which signals through adenosine receptors to inhibit platelet activation. | |
| Heat shock protein 27HSPB1 | protein | 5 | — | ◆ | Heat shock protein 27 modulates platelet cytoskeletal dynamics and inhibits thrombotic responses, potentially stabilizing platelet function during atherothrombo | |
| serotonin | metabolite | 4 | 2 | — | Serotonin is stored in and released from platelet α-granules during activation, promoting vasoconstriction and platelet–platelet recruitment at the thrombotic s | |
| Annexin VANXA5 | protein | 4 | — | ◆ | Annexin V enhances platelet and leukocyte microparticle–mediated thrombin generation during acute coronary thrombosis. | |
| Beta-2-glycoprotein IAPOH | protein | 4 | — | ◆ | Beta-2-glycoprotein I complexes with oxidized LDL in atherosclerotic lesions and is targeted by antiphospholipid antibodies to activate thrombosis. | |
| Cathelicidin Antimicrobial PeptideCAMP | protein | 4 | — | ◆ | CAMP mediates antiplatelet signaling and immune regulation during acute myocardial injury. | |
| CD42aGP9 | protein | 4 | — | ◆ | CD42a-positive small extracellular vesicles are released during platelet activation and reflect early thrombus formation in acute MI. | |
| Dipeptidyl peptidase-4DPP4 | protein | 4 | — | ✦◆ | DPP-4 regulates GLP-1 stability and directly modulates platelet aggregation and endothelial function in MI. | |
| Glycoprotein VGP5 | protein | 4 | — | ◆ | GP5 downregulation in NSTEMI reflects enhanced platelet activation, consumption, and thrombin-driven coagulation. | |
| GPV | protein | 4 | — | — | GPV is a thrombin-activated platelet membrane protein released during platelet activation, indicating both thrombin generation and platelet responsiveness at th | |
| Mean Platelet Volume | other | 4 | — | — | Mean platelet volume reflects platelet function and predicts thrombotic recurrence in acute coronary syndromes. | |
| miR-21 | rna | 4 | — | — | miR-21 is elevated during acute MI, promoting platelet activation and aggregation while amplifying cardiomyocyte injury responses. | |
| Mitogen-Activated Protein Kinase p38MAPK14 | protein | 4 | — | ◆ | MAPK14 (p38α) regulates platelet activation and inflammatory responses, contributing to thrombotic amplification post-plaque rupture. | |
| PAC-1 | protein | 4 | — | — | PAC-1 is a monoclonal antibody probe binding the activated (ligand-receptive) conformation of platelet integrin GPIIb-IIIa, directly reporting platelet activati | |
| Phenylacetylglutamine | metabolite | 4 | — | — | PAGln derived from microbiota metabolism promotes platelet activation and thrombotic response, increasing MI risk in rupture-prone plaques. | |
| Phospholipase Cγ2PLCG2 | gene | 4 | — | ◆ | PLCG2 transduces GPVI-collagen signaling amplifying platelet activation and aggregation. | |
| Platelet-activating factor | lipid | 4 | — | — | PAF amplifies platelet activation and recruits leukocytes in coronary thrombogenesis. | |
| Platelet-derived microparticles | complex | 4 | — | — | Platelet-derived vesicles released during platelet activation that propagate tissue-factor-driven thrombus formation. | |
| Spleen tyrosine kinaseSYK | gene | 4 | — | ◆ | Syk tyrosine kinase transduces GPVI-collagen signaling driving platelet activation and adhesion. | |
| SRC tyrosine kinaseSRC | protein | 4 | — | ◆ | SRC mediates platelet activation and platelet-leukocyte crosstalk via downstream phosphorylation, amplifying thrombotic response at the ruptured atherosclerotic | |
| VimentinVIM | protein | 4 | — | ◆ | Vimentin is released from the platelet cytoskeleton during activation and reflects both platelet involvement and vascular inflammation. | |
| Cytochrome P450 2C19CYP2C19 | gene | 3 | 8 | ✦◆ | CYP2C19 genetic variants regulate clopidogrel activation, modulating platelet aggregation inhibition and stent thrombosis risk after coronary intervention. | |
| Aldehyde Dehydrogenase 2ALDH2 | gene | 3 | — | ✦◆ | ALDH2 controls acetaldehyde and reactive-aldehyde detoxification, regulating platelet activation state and thrombotic predisposition in acute coronary events. | |
| Cathepsin GCTSG | protein | 3 | — | ◆ | Cathepsin G amplifies platelet recruitment and thrombin generation via ADP release and coagulation cascade activation. | |
| Citrullinated Histone H3 | peptide | 3 | — | — | Citrullinated histone H3 from neutrophil extracellular traps drives platelet activation and thrombus formation in STEMI. | |
| CLEC-2CLEC1B | protein | 3 | — | ◆ | Platelet surface receptor mediating collagen recognition and activation during thrombus formation. | |
| Complement component 5a | peptide | 3 | — | — | C5a recruits neutrophils and activates platelets, amplifying thromboinflammatory response in acute MI. | |
| FcγRIIaFCGR2A | protein | 3 | — | ◆ | Fc receptor on platelets mediating immune-complex-driven platelet aggregation and thrombotic amplification. | |
| Fermitin family homolog 3FERMT3 | protein | 3 | — | ◆ | FERMT3 is a focal adhesion protein that mediates platelet integrin activation and firm adhesion, with elevated expression marking plaque erosion and thrombosis. | |
| Glucagon-like peptide-1GCG | peptide | 3 | — | ✦◆ | GLP-1 exerts anti-thrombotic and anti-inflammatory effects, reducing platelet aggregation and endothelial activation in MI pathogenesis. | |
| Integrin alpha-2ITGA2 | protein | 3 | — | ◆ | Integrin mediating platelet adhesion to collagen on exposed vessel wall; critical for thrombus formation. | |
| miR-150 | rna | 3 | — | — | miRNA modulating platelet function and ventricular remodeling following acute ischemic injury. | |
| miR-223 | rna | 3 | — | — | miR-223 dysregulation in acute coronary events amplifies platelet activation and leukocyte recruitment, predicting post-MI mortality. | |
| Protein kinase APRKACA | protein | 3 | — | ◆ | Cardiac signaling kinase whose cAMP-dependent activity suppresses platelet activation and thrombus formation through anti-aggregatory pathways. | |
| VinculinVCL | protein | 3 | — | ◆ | Vinculin is released from platelet cytoskeleton during activation and aggregation, marking platelet involvement in acute coronary thrombosis. | |
| Hemoglobin | protein | 2 | 2 | — | Released hemoglobin amplifies oxidative stress and promotes platelet activation and thrombosis in acute coronary occlusion. | |
| 12-HETE | metabolite | 2 | — | — | 12-HETE is an eicosanoid mediator that activates platelets and amplifies oxidative stress during acute MI. | |
| 12-LipoxygenaseALOX12 | gene | 2 | — | ◆ | 12-LOX catalyzes arachidonic acid metabolism toward pro-thrombotic lipid mediators that amplify platelet response. | |
| Actin, BetaACTB | protein | 2 | — | ◆ | Beta-actin is essential for platelet shape change, cytoskeletal reorganization during activation, and the adhesion-molecule-mediated tethering to exposed collag | |
| ADAM10ADAM10 | protein | 2 | — | ◆ | ADAMTS family protease mediating ectodomain shedding of platelet and endothelial activation markers. | |
| ADAM17ADAM17 | protein | 2 | — | ◆ | ADAMTS family protease releasing soluble forms of adhesion receptors and modulating platelet-endothelial interactions. | |
| Atypical Chemokine Receptor 3ACKR3 | gene | 2 | — | ◆ | ACKR3 dampens platelet activation and thromboinflammatory signaling, protecting against thrombus amplification. | |
| CD66bCEACAM8 | protein | 2 | — | ◆ | CD66b-positive neutrophil microparticles and extracellular traps amplify platelet activation and thrombus propagation in STEMI. | |
| CD84 | protein | 2 | — | — | CD84 mediates platelet-to-platelet adhesion and thrombus stabilization during coronary occlusion. | |
| CEACAM1 (carcinoembryonic antigen-related cell adhesion molecule 1)CEACAM1 | gene | 2 | — | ◆ | Cell-adhesion molecule functioning as a negative regulator of platelet activation and correlating with aggregation capacity. | |
| Collagen | protein | 2 | — | — | Collagen exposure following fibrous-cap rupture or endothelial erosion triggers GPVI-mediated platelet adhesion and the initiation of thrombosis in Type 1 MI. | |
| Complement component 3a | peptide | 2 | — | — | C3a activates complement-driven platelet recruitment and thromboinflammatory cascade in coronary thrombosis. | |
| dsDNA | other | 2 | — | — | Circulating dsDNA from neutrophil extracellular traps marks platelet-leukocyte activation and correlates with myocardial injury magnitude. | |
| Extracellular Signal-Regulated Kinase 1MAPK3 | protein | 2 | — | ◆ | ERK1 participates in platelet activation signaling and integrates with p38 pathways to amplify platelet recruitment and aggregation. | |
| Fyn KinaseFYN | protein | 2 | — | ◆ | FYN amplifies platelet activation via GPVI signaling and supports platelet-leukocyte crosstalk, driving thrombotic occlusion. | |
| glycocalicin | protein | 2 | — | — | Glycocalicin is the soluble ectodomain of platelet GPIbα shed during platelet activation, reflecting vWF-mediated platelet tethering and adhesion to injured end | |
| GNAQGNAQ | gene | 2 | — | ◆ | GNAQ encodes a Gαq protein essential for platelet signaling and thrombus formation, directly driving the thrombotic occlusion phase of Type 1 MI. | |
| Integrin alphaIIbbeta3 | protein | 2 | — | — | Platelet glycoprotein integrin mediating fibrinogen-dependent platelet–platelet aggregation and thrombus propagation. | |
| L-tryptophan | metabolite | 2 | — | — | L-tryptophan dysregulation reflects platelet activation and thrombotic stress in acute coronary syndrome. | |
| P-selectin (CD62P) | protein | 2 | — | — | P-selectin (CD62P) mediates platelet–leukocyte adhesion and tethering, amplifying thromboinflammation in Type 1 MI. | |
| Phosphatidylinositol 3-kinase | gene | 2 | — | — | PI3K signaling drives platelet activation and endothelial progenitor cell mobilization, regulating thrombotic and reparative responses. | |
| Phosphatidylinositol 3-kinase class IB catalytic subunitPIK3CB | gene | 2 | — | ◆ | PIK3CB promotes phosphatidylinositol-3-kinase signaling downstream of CD40L, enhancing platelet activation and thrombus formation. | |
| Platelet-derived growth factor BB | protein | 2 | — | — | PDGF-BB released from activated platelets amplifies plaque inflammation and predicts microvascular thrombosis and no-reflow in acute coronary occlusion. | |
| Platelet-derived growth factor-APDGFA | protein | 2 | — | ◆ | PDGF-A from activated platelets promotes vascular inflammation and plaque destabilization, amplifying thrombotic response in STEMI. | |
| RhoARHOA | protein | 2 | — | ◆ | RhoA GTPase mediates platelet activation and endothelial dysfunction in Type 1 MI. | |
| Semaphorin 7ASEMA7A | protein | 2 | — | ◆ | Sema7A bridges platelet activation and monocyte recruitment, amplifying thrombo-inflammatory responses during acute MI and reperfusion injury. | |
| SLAM-Associated ProteinSH2D1A | protein | 2 | — | — | SAP mediates platelet activation and platelet–leukocyte aggregation, amplifying thrombotic and inflammatory responses during acute coronary thrombosis. | |
| SLP-76LCP2 | protein | 2 | — | — | SLP-76 scaffolds GPVI signaling to couple collagen recognition to platelet secretion and aggregation. | |
| Transgelin-2TAGLN2 | protein | 2 | — | ◆ | TAGLN2 dysregulation in ACS platelets reflects aberrant cytoskeletal remodeling in atherothrombotic activation. | |
| β-Thromboglobulin | protein | 2 | — | — | β-Thromboglobulin is released during platelet activation and aggregation, marking the initiation of thrombotic cascade in acute MI. | |
| LIGHTTNFSF14 | protein | 1 | 1 | ◆ | LIGHT (TNFSF14) promotes platelet adhesion and endothelial activation, facilitating leukocyte recruitment and thromboinflammatory cascade. | |
| miR-126MIR126 | rna | 1 | 1 | — | miR-126 released from activated platelets modulates adhesion and aggregation, reflecting thrombotic MI burden. | |
| PGD2 | metabolite | 1 | 1 | — | PGD2 is an anti-platelet prostanoid whose post-PCI reduction indicates resolution of acute thrombus-associated inflammation. | |
| Platelet extracellular vesicles | other | 1 | 1 | — | Platelet-derived extracellular vesicles released during activation amplify thrombin generation and fibrin formation, contributing to occlusive thrombus propagat | |
| TIPS | rna | 1 | 1 | — | Platelet-derived thromboinflammatory RNA signature that integrates platelet activation and inflammatory signals associated with MI risk. | |
| 12-HETrE | metabolite | 1 | — | — | 12-HETrE is a lipid metabolite that suppresses platelet adhesion and activation in response to vessel injury. | |
| 13-HODE | metabolite | 1 | — | — | 13-HODE, an oxidized linoleic acid metabolite, suppresses platelet aggregation and protects against thrombosis in Type 1 MI. | |
| 18-HEPE | metabolite | 1 | — | — | 18-HEPE, derived from eicosapentaenoic acid, exerts antiplatelet effects limiting platelet-driven thrombosis. | |
| 5-oxo-ETE | metabolite | 1 | — | — | 5-oxo-ETE is an arachidonic-acid-derived eicosanoid that promotes leukocyte infiltration and myocardial injury during acute myocardial infarction. | |
| 9-HODE | metabolite | 1 | — | — | 9-HODE, an oxidized linoleic acid metabolite, inhibits platelet aggregation and reduces thrombotic burden in acute coronary events. | |
| ACAD10ACAD10 | protein | 1 | — | ✦◆ | ACAD10 controls platelet mitochondrial homeostasis and activation state, modulating the thrombotic response to vascular injury. | |
| Actin, Gamma 1ACTG1 | protein | 1 | — | ◆ | Gamma-actin is critical for platelet contractile responses, morphological changes during activation, and stable adhesion to thrombogenic surfaces. | |
| Adrenergic Receptor Alpha-2AADRA2A | gene | 1 | — | ◆ | ADRA2A signaling transduces PAGln-driven platelet activation and leukocyte recruitment in atherothrombotic cascades. | |
| Adrenergic Receptor Alpha-2BADRA2B | gene | 1 | — | ◆ | ADRA2B signaling transduces PAGln effects on platelet response and vascular inflammation. | |
| ATP1A1ATP1A1 | gene | 1 | — | ◆ | ATP1A1 encodes Na/K-ATPase α1, which maintains platelet ion homeostasis and contractility, supporting but not directly driving thrombotic activation. | |
| ATP6V1G2 (vacuolar H+ ATPase subunit G2)ATP6V1G2 | gene | 1 | — | ◆ | Vacuolar H+ ATPase subunit correlating with platelet aggregation capacity via granule acidification. | |
| Aurora kinase BAURKB | gene | 1 | — | ◆ | Aurora kinase B elevated in STEMI platelets, regulating platelet cytokinesis and activation dynamics. | |
| AutotaxinENPP2 | protein | 1 | — | ◆ | Autotaxin-LPA axis promotes platelet activation and plaque inflammation in atherothrombosis. | |
| B-cell Activating FactorTNFSF13B | protein | 1 | — | ◆ | BAFF, released from activated platelets, amplifies B-cell and vascular inflammation in atherothrombotic coronary disease. | |
| C4d | protein | 1 | — | — | C4d deposition marks platelet activation and complement engagement in arterial thrombosis. | |
| CACNA1ICACNA1I | gene | 1 | — | ◆ | CACNA1I encodes a T-type calcium channel contributing to platelet activation signaling, though not a primary thrombotic driver in Type 1 MI. | |
| CD226 Antigen (DNAM-1)CD226 | protein | 1 | — | ◆ | CD226 upregulation enhances platelet-mediated thrombosis in clopidogrel-resistant ACS and Type 1 MI. | |
| CD235aGYPA | protein | 1 | — | ✦◆ | CD235a on erythrocyte-derived microparticles signals platelet activation and thrombus propagation during coronary occlusion. | |
| CD41+ microparticles | complex | 1 | — | — | CD41+ microparticles reflect platelet activation and contribute to thrombin generation and thrombus formation post-plaque rupture. | |
| CD61 (β3 integrin subunit) | protein | 1 | — | — | CD61 is a structural component of integrin αIIbβ3 and serves as a pan-platelet marker. | |
| cGMP | metabolite | 1 | — | — | cGMP exerts inhibitory signaling that suppresses platelet aggregation and thrombus formation. | |
| cGMP-dependent protein kinase IPRKG1 | protein | 1 | — | ◆ | PRKG1 phosphorylates substrates that inhibit platelet activation, reducing thrombotic risk in atherothrombosis. | |
| circular RNAs | rna | 1 | — | — | Circular RNAs are platelet-derived microvesicle markers released during platelet activation and thrombus formation. | |
| citrullinated histone H3HIST1H3A | protein | 1 | — | — | Citrullinated histone H3 from neutrophil extracellular traps is incorporated into coronary thrombi, promoting platelet activation and coagulation. | |
| Cyclic GMP-AMP SynthaseCGAS | protein | 1 | — | ◆ | cGAS senses platelet-associated dsDNA and drives thromboinflammatory platelet activation. | |
| Cyclophilin DPPIF | protein | 1 | — | ◆ | Cyclophilin D regulates platelet necrosis and activation, modulating thrombus formation and myocardial injury signaling. | |
| Death inducer obliterator 1DIDO1 | protein | 1 | — | — | DIDO1 is a circulating biomarker upregulated in STEMI plasma, reflecting platelet activation and thrombotic burden during acute coronary occlusion. | |
| DHETs | metabolite | 1 | — | — | DHETs, the hydrolyzed metabolites of EETs, accumulate post-PCI and mark active eicosanoid-mediated vascular repair and endothelial recovery. | |
| Diacylglycerol kinaseDGKA | protein | 1 | — | ◆ | Diacylglycerol kinase dysregulation promotes platelet hyperreactivity in Type 1 MI. | |
| Dok-2DOK2 | protein | 1 | — | ◆ | Dok-2 fine-tunes GPVI-driven platelet activation, affecting thrombus propagation kinetics. | |
| EETs | metabolite | 1 | — | — | EETs are vasoprotective epoxyeicosatrienoic acids whose post-PCI elevation indicates restoration of endothelial-protective eicosanoid metabolism. | |
| enoyl-CoA hydratase domain-containing protein 3ECHDC3 | gene | 1 | — | ◆ | Metabolic enzyme elevated in STEMI platelets with undefined role in platelet function. | |
| ERK1/2 | protein | 1 | — | — | ERK1/2 kinases transduce activation signals driving platelet aggregation and thrombus formation. | |
| ERMERM | protein | 1 | — | — | ERM proteins organize platelet cytoskeleton and membrane dynamics during activation. | |
| Extracellular signal-regulated kinase 2MAPK1 | protein | 1 | — | ◆ | ERK2 transduces p38 signaling to promote platelet activation and thrombus formation in coronary thrombosis. | |
| F-box and leucine-rich repeat protein 4FBXL4 | gene | 1 | — | — | F-box ubiquitin ligase elevated in STEMI platelets, involved in platelet activation signaling. | |
| FcRγ-chain | protein | 1 | — | — | FcRγ-chain couples GPVI collagen sensing to PLCγ2 and downstream platelet activation. | |
| FKBP5 (FK506-binding protein 5)FKBP5 | gene | 1 | — | ◆ | Immunophilin co-chaperone elevated in STEMI platelets, modulating stress response and protein folding. | |
| FYVE, RhoGEF and PH Domain Containing 6FGD6 | protein | 1 | — | ✦ | FGD6, elevated during acute MI, may regulate small-GTPase signaling in platelet or endothelial dysfunction. | |
| Glutathione-S-transferaseGSTA1 | protein | 1 | — | ◆ | Glutathione-S-transferase reflects platelet antioxidant response and oxidative stress during acute coronary thrombosis. | |
| Glycoprotein Ib alpha | protein | 1 | — | — | GPIbα is the vWF-binding platelet receptor that initiates platelet tethering to exposed subendothelial collagen and injured endothelium, triggering downstream a | |
| Glycoprotein Ib-V-IX complex | protein | 1 | — | — | Glycoprotein Ib-V-IX mediates initial platelet adhesion to von Willebrand factor on exposed subendothelium, initiating thrombus formation. | |
| Glycoprotein Ib-βGP1BB | gene | 1 | — | ◆ | GP1BB prothrombotic variants enhance platelet tethering to exposed collagen/vWF and increase thrombotic risk. | |
| Glycoursodeoxycholic acid | metabolite | 1 | — | — | Glycoursodeoxycholic acid suppresses platelet activation, reducing Type 1 MI thrombus burden. | |
| GPC5GPC5 | protein | 1 | — | ◆ | GPC5 is a surface proteoglycan regulating adhesion and coagulation; protective variants reduce sudden cardiac arrest risk in MI. | |
| GPIb-alpha | protein | 1 | — | — | GPIb-alpha binds von Willebrand factor, initiating platelet adhesion and aggregation at sites of endothelial injury. | |
| Gremlin-1 | protein | 1 | — | — | Gremlin-1, a platelet-derived cytokine, promotes platelet activation and vascular inflammation during acute coronary syndrome. | |
| Gα12/13 proteinGNA12 | protein | 1 | — | ◆ | GNA12/13-coupled pathways drive shape change and aggregation responses to thrombin and other platelet agonists. | |
| Gαi proteinGNAI | protein | 1 | — | — | GNAI-coupled receptors transduce anti-aggregatory signals that suppress platelet activation during thrombus formation. | |
| HDL2 | lipoprotein | 1 | — | — | HDL2 exerts antiplatelet and antithrombotic effects, opposing platelet activation at the thrombotic phase of Type 1 MI. | |
| HeparanaseHPSE | protein | 1 | — | ◆ | Heparanase degrades subendothelial heparan sulfate, promoting platelet and leukocyte infiltration and thrombus expansion in STEMI. | |
| Histamine | metabolite | 1 | — | — | Histamine dampens platelet activation and thromboinflammation, protecting against coronary microthrombosis in acute MI. | |
| Histidine DecarboxylaseHDC | gene | 1 | — | ◆ | HDC catalyzes histamine synthesis, modulating platelet activation and plaque inflammation in atherothrombotic disease. | |
| Histone H1H1F0 | protein | 1 | — | — | Circulating histone H1 from NETs activates platelets and endothelium, amplifying thrombus formation. | |
| HPS3HPS3 | gene | 1 | — | ◆ | HPS3 controls platelet dense-granule biogenesis and release, modulating ADP-driven platelet activation during thrombotic events. | |
| Integrin alpha | protein | 1 | — | — | Integrin alpha subunits heterodimerize with integrin beta-2 to mediate platelet adhesion and aggregation in thrombosis. | |
| Integrin beta-1ITGB1 | protein | 1 | — | ◆ | Integrin β1 mediates leukocyte and platelet recruitment to inflamed and eroding plaques. | |
| KCNE1 (potassium channel auxiliary subunit)KCNE1 | gene | 1 | — | ◆ | Ion-channel auxiliary subunit elevated in STEMI platelets, potentially modulating platelet physiology. | |
| Linker for activation of T cellsLAT | protein | 1 | — | ◆ | LAT mediates downstream signaling from GPVI collagen receptor, propagating platelet activation and adhesion to exposed subendothelial matrix. | |
| Lyn kinaseLYN | gene | 1 | — | ◆ | LYN phosphorylates adapter proteins downstream of GPVI collagen receptor, initiating the signaling cascade that drives platelet activation and thrombus formatio | |
| Lysosomal-associated membrane protein 1LAMP1 | protein | 1 | — | ◆ | Exposed on the platelet surface upon α-granule exocytosis during platelet activation and thrombus formation. | |
| Manganese superoxide dismutaseSOD2 | protein | 1 | — | ◆ | Manganese superoxide dismutase reflects platelet antioxidant defense and oxidative stress during acute coronary activation. | |
| MAPK-activated protein kinase 2MAPKAPK2 | protein | 1 | — | ◆ | MAPKAPK2 amplifies p38-mediated platelet activation and α-granule release driving thrombotic response. | |
| miR-143-3p | rna | 1 | — | — | miR-143-3p targets vascular proteins involved in smooth-muscle contractility and platelet adhesion, modulating the thrombotic response to plaque rupture. | |
| miR-145-5p | rna | 1 | — | — | miR-145-5p suppresses vascular targets that regulate endothelial barrier function and platelet activation during thromboinflammation. | |
| miR-148b-3pMIR148B | rna | 1 | — | — | microRNA regulating platelet activation and aggregation signals in thrombotic cascade. | |
| miR-151a-5pMIR151A | rna | 1 | — | — | microRNA regulating platelet activation and aggregation signals in thrombotic cascade. | |
| miR-199a-3p | rna | 1 | — | — | miR-199a-3p is a circulating microRNA biomarker of platelet activation that regulates genes governing thromboinflammatory responses. | |
| Mitochondrial ATP synthase subunit 6MT-ATP6 | gene | 1 | — | ◆ | Mitochondrial DNA methylation in platelets indicates altered energy metabolism and platelet activation status in MI. | |
| Mitochondrial Cytochrome c Oxidase Subunit 1MT-CO1 | gene | 1 | — | ◆ | MT-CO1 methylation changes reflect platelet activation and mitochondrial stress in acute MI. | |
| Mitochondrial Cytochrome c Oxidase Subunit 2MT-CO2 | gene | 1 | — | ◆ | MT-CO2 methylation status serves as a marker of platelet mitochondrial dysfunction in MI. | |
| Mitochondrial Cytochrome c Oxidase Subunit 3MT-CO3 | gene | 1 | — | ◆ | MT-CO3 methylation reflects platelet metabolic activation and oxidative stress in acute MI. | |
| Mitochondrial NADH dehydrogenase subunit 5MT-ND5 | gene | 1 | — | ◆ | Mitochondrial DNA methylation in platelets serves as a marker of platelet metabolic status and activation during thrombotic events. | |
| Mitochondrial tRNA leucineMT-TL1 | rna | 1 | — | — | Mitochondrial tRNA methylation patterns in platelets reflect mitochondrial function during thrombotic activation. | |
| MOB3CMOB3C | gene | 1 | — | — | MOB3C may regulate platelet–leukocyte interactions and vascular cell adhesion in thrombotic response. | |
| MST1RMST1R | gene | 1 | — | ◆ | MST1R (RON) promotes platelet activation and leukocyte recruitment in atherothrombotic cascades. | |
| Myosin heavy chain 9MYH9 | protein | 1 | — | ◆ | MYH9 is a focal adhesion protein that mediates platelet contractility and firm adhesion to exposed collagen/vWF during coronary thrombus formation. | |
| Neutrophil Activating Protein-2CXCL7 | protein | 1 | — | — | Neutrophil Activating Protein-2 is a platelet-derived chemokine promoting platelet activation and leukocyte recruitment. | |
| NINJ1NINJ1 | protein | 1 | — | ◆ | Platelet-intrinsic protein mediating platelet activation and membrane perturbation during thrombus formation. | |
| Nucleosome | complex | 1 | — | — | Nucleosome complexes released in neutrophil extracellular traps promote platelet activation and thrombus formation at the site of plaque rupture. | |
| Oligophrenin-1OPHN1 | protein | 1 | — | ◆ | Oligophrenin-1 transduces Rev-erb α signaling to enhance platelet activation in MI. | |
| OXE-R | protein | 1 | — | — | OXE-R (oxoeicosanoid receptor) transduces 5-oxo-ETE signaling to promote leukocyte recruitment and myocardial damage; a candidate cardioprotective target. | |
| P-selectin+ microparticles | complex | 1 | — | — | P-selectin+ microparticles are released during platelet activation and mediate leukocyte adhesion at sites of arterial injury. | |
| P2X1 ReceptorP2RX1 | protein | 1 | — | ◆ | P2X1 receptor mediates ATP-dependent rapid platelet activation and calcium influx during thrombus formation. | |
| P2Y1 ReceptorP2RY1 | protein | 1 | — | ◆ | P2Y1 receptor mediates ADP-dependent platelet activation and thrombus formation at the site of plaque rupture. | |
| PAR4 | protein | 1 | — | — | PAR4 is a thrombin-activated platelet receptor whose signaling drives platelet shape change, aggregation, and secretion during coronary thrombosis. | |
| Parvin alphaPARVA | protein | 1 | — | ◆ | PARVA is a focal adhesion protein that anchors the actin cytoskeleton in platelets, supporting firm adhesion and thrombotic response at the injury site. | |
| PDGFB (platelet-derived growth factor subunit B)PDGFB | gene | 1 | — | ◆ | Platelet-derived growth factor subunit correlating with platelet aggregation and involved in vascular responses to injury. | |
| PGE2 | metabolite | 1 | — | — | PGE2 is an anti-platelet prostanoid whose post-intervention decline reflects resolution of acute platelet activation in STEMI. | |
| Phenylacetylglycine | metabolite | 1 | — | — | PAGly augments platelet activation and adhesion in response to exposed plaque substrate. | |
| Phosphatidylcholine 18:0 | lipid | 1 | — | — | PC18:0 activates platelet adhesion and aggregation during acute thrombotic events. | |
| Phospholipase Cγ2 | protein | 1 | — | — | PLCγ2 activation is a critical branch point in collagen/GPVI-triggered platelet activation and thrombus formation. | |
| Platelet factor 4 | protein | 1 | — | — | Platelet factor 4 released during platelet activation promotes further platelet recruitment and enhances tissue-factor-driven coagulation. | |
| Platelet glycoprotein Ib/V/IX complex | complex | 1 | — | — | GPIb/V/IX mediates the initial catch-bond interaction between platelets and von Willebrand factor at sites of endothelial injury. | |
| Platelet-Derived Growth Factor CPDGFC | protein | 1 | — | ◆ | PDGFC promotes platelet activation and aggregation at the site of vascular injury. | |
| Profilin-1PFN1 | protein | 1 | — | ◆ | Actin-nucleating protein released during platelet activation and thrombus formation. | |
| Protein Disulfide IsomeraseP4HB | protein | 1 | — | ◆ | PDI catalyzes disulfide bond formation in platelet integrins and coagulation factors, promoting thrombosis. | |
| Protein disulfide-isomerase A3PDIA3 | protein | 1 | — | ◆ | PDIA3 release during acute coronary events promotes platelet adhesion and thrombus propagation. | |
| Protein Kinase C AlphaPRKCA | protein | 1 | — | ◆ | PKCα phosphorylates downstream effectors of platelet activation, promoting adhesion and thrombus formation. | |
| Protein phosphatase 2C metazoanPPM1B | protein | 1 | — | ◆ | PP2Cm activates branched-chain amino acid catabolism, altering amino-acid-driven signaling that modulates platelet activation and thrombotic risk. | |
| RAS-related protein 1BRAP1B | protein | 1 | — | ◆ | RAP1B is a small GTPase that regulates platelet integrin activation and focal adhesion formation, enabling platelet tethering and stable adhesion during coronar | |
| Rev-erb αNR1D1 | protein | 1 | — | ◆ | Rev-erb α controls circadian platelet reactivity, potentiating Type 1 MI thrombosis. | |
| rLj-RGD3 | protein | 1 | — | — | rLj-RGD3 inhibits platelet adhesion and aggregation by blocking integrin-mediated interaction with the thrombogenic substrate. | |
| sC5b-9 | protein | 1 | — | — | sC5b-9 (terminal complement complex) activates platelets and endothelium, bridging complement activation to thrombosis. | |
| SCUBE1 | protein | 1 | — | — | SCUBE1 is a soluble protein released from platelet α-granules during activation, serving as a marker of platelet secretion and thrombotic state initiation. | |
| Serum and Glucocorticoid-regulated Kinase 1SGK1 | protein | 1 | — | ◆ | SGK1 promotes platelet activation and thrombotic responses in acute coronary syndromes. | |
| SLC2A3 (glucose transporter 3)SLC2A3 | gene | 1 | — | ◆ | Glucose transporter 3 correlating with platelet aggregation function through metabolic substrate availability. | |
| SNAP29SNAP29 | protein | 1 | — | ◆ | SNAP29 orchestrates α-granule exocytosis and dense-granule release, amplifying platelet recruitment and thrombus stabilization. | |
| soluble semaphorin 4DSEMA4D | protein | 1 | — | ◆ | Soluble semaphorin 4D, a platelet-derived mediator, predicts thrombus burden and major adverse cardiac events. | |
| soluble TREM-like transcript-1TREML1 | protein | 1 | — | ◆ | sTLT-1 shedding marks platelet activation and thrombotic burden in coronary disease. | |
| Src family kinases | protein | 1 | — | — | Src family kinases transduce GPVI collagen-binding signals, driving platelet activation and thrombus propagation at the ruptured plaque. | |
| ST3 beta-galactoside alpha-2,3-sialyltransferase 6ST3GAL6 | protein | 1 | — | ◆ | ST3GAL6 regulates platelet adhesion molecule glycosylation, affecting platelet aggregation capacity. | |
| ST6Gal-1ST6GAL1 | protein | 1 | — | ◆ | ST6Gal-1 modulates platelet activation through sialic-acid glycosylation of adhesion ligands. | |
| Stimulator of Interferon GenesTMEM173 | protein | 1 | — | — | STING transduces cGAS-detected dsDNA signals to activate platelets and promote thrombus formation. | |
| STX6STX6 | protein | 1 | — | ◆ | STX6 regulates intracellular calcium mobilization; variants influence platelet activation kinetics and thrombotic response. | |
| Synaptotagmin 11SYT11 | protein | 1 | — | ◆ | SYT11 regulates exocytosis and cell–cell communication implicated in thromboinflammatory responses. | |
| TAO kinase 2TAOK2 | gene | 1 | — | ◆ | Serine-threonine kinase elevated in STEMI platelets, involved in platelet signaling cascades. | |
| ThrombopoietinTHPO | protein | 1 | — | ◆ | Thrombopoietin activates platelets and couples thrombosis to inflammation, driving coronary thrombus formation. | |
| Thrombopoietin ReceptorMPL | protein | 1 | — | ◆ | MPL signaling modulates platelet mass and functional state, influencing thrombotic response at coronary lesion. | |
| TNF receptor superfamily member 10CTNFRSF10C | protein | 1 | — | ◆ | TNFRSF10C acts as a TNF superfamily receptor contributing to inflammatory signaling and platelet-leukocyte crosstalk in coronary thrombus. | |
| Tropomodulin-3TMOD3 | protein | 1 | — | — | Tropomodulin-3 propionylation at lysine 255 couples branched-chain amino acid metabolism to platelet activation signaling. | |
| Vasodilator-stimulated phosphoprotein | protein | 1 | — | — | VASP phosphorylation state reflects endothelial nitric oxide signaling and serves as a marker of platelet activation resistance. | |
| vitamin D receptorVDR | protein | 1 | — | ◆ | VDR regulates platelet activation and inflammatory responses, modulating thrombosis in acute coronary syndrome. | |
| Xanthine oxidoreductase | protein | 1 | — | — | Xanthine oxidoreductase activity modulates platelet function through redox-sensitive signaling pathways. | |
| Y RNAs | rna | 1 | — | — | Y RNAs are platelet-derived RNA fragments released during platelet activation and aggregation at the thrombotic site. | |
| β-tubulinTUBB | protein | 1 | — | ✦◆ | β-tubulin is released from the platelet cytoskeleton during shape change and activation in acute coronary events. | |
| Abl Interactor 2ABI2 | gene | — | — | ✦◆ | ABI2 couples receptor signaling to actin remodeling; essential for platelet spreading and thrombus formation. | |
| Docking Protein 6DOK6 | gene | — | — | ✦ | DOK proteins regulate platelet adhesion and integrin-mediated signaling in thrombosis. | |
| Non-catalytic tyrosine-protein kinase adaptor NCK1NCK1 | gene | — | — | ✦◆ | NCK1 couples receptor tyrosine kinases to actin remodeling; regulates platelet activation and adhesion signaling. | |
| Phospholipase C beta 2PLCB2 | gene | — | — | ✦◆ | Phospholipase C mediates platelet G-protein signaling and platelet activation/aggregation. | |
| Ras Association (RalGDS/AF-6) And Pleckstrin Homology Domains 1RAPH1 | gene | — | — | ✦◆ | RAPH1 mediates Ras-dependent adhesion signaling; promotes integrin clustering and platelet-endothelial interaction. | |
| RasGEF Domain Family Member 1BRASGEF1B | gene | — | — | ✦◆ | RASGEF1B activates Rap1 GTPase, promoting integrin clustering and platelet/leukocyte adhesion. | |
| Tubulin beta-1TUBB1 | gene | — | — | ✦◆ | TUBB1 is essential for megakaryocyte and platelet microtubule organization; mutations impair platelet granule cargo secretion and hemostasis. | |
| Tubulin beta-4BTUBB4B | gene | — | — | ✦◆ | TUBB4B maintains platelet cytoskeleton and granule architecture; variants affect platelet activation, aggregation, and thrombotic response. | |
| Vesicle Associated Membrane Protein 5VAMP5 | gene | — | — | ✦◆ | VAMP5 mediates α-granule and dense-granule release in platelet activation; critical for thrombus formation. |
Thromboxane amplification
Thromboxane / COX-115| Molecule | Type | Conf. | Refs | Trials | Evidence | Mechanism |
|---|---|---|---|---|---|---|
| Thromboxane B2 | metabolite | 15 | — | — | Thromboxane B2 is the stable inactive metabolite of thromboxane A2, a COX-1-generated eicosanoid that amplifies platelet recruitment and aggregation. | |
| arachidonic acid | metabolite | 13 | — | — | Arachidonic acid elevation drives thromboxane-A2 generation and eicosanoid-mediated platelet aggregation and inflammation in acute MI. | |
| COX-2PTGS2 | gene | 7 | — | ✦◆ | COX-2 catalyzes thromboxane-A2 and prostacyclin synthesis, driving platelet activation and inflammation in Type 1 MI. | |
| Cyclooxygenase-1PTGS1 | gene | 6 | — | ✦◆ | COX-1 generates thromboxane-A2, which amplifies platelet recruitment and aggregation during coronary thrombosis. | |
| Thromboxane A2 | metabolite | 4 | — | — | Thromboxane A2 amplifies platelet activation and aggregation through COX-1 pathway, driving thrombus formation and coronary occlusion. | |
| cyclooxygenase | protein | 2 | 1 | — | Cyclooxygenase-1 catalyzes arachidonic acid conversion to thromboxane-A2, driving platelet recruitment and coronary thrombosis. | |
| 11-dehydro-thromboxane B2 | metabolite | 2 | — | — | Stable metabolite of thromboxane-A2 that quantifies COX-1-dependent platelet activation amplifying thrombosis. | |
| 11-dehydrothromboxane B2 | metabolite | 1 | — | — | 11-dehydrothromboxane B2 is the stable metabolite of thromboxane A2, marking COX-1-driven platelet activation and recruitment. | |
| 11-dehydroTxB2 | metabolite | 1 | — | — | 11-dehydroTxB2 is the stable urinary metabolite of thromboxane-A2, quantifying COX-1-driven platelet amplification in coronary thrombosis. | |
| 2,3-dinor-thromboxane B2 | metabolite | 1 | — | — | 2,3-dinor-thromboxane B2 is a urinary metabolite reflecting systemic thromboxane-A2 production, a COX-1-dependent amplifier of platelet recruitment and aggregat | |
| C20:4 (arachidonic acid) | metabolite | 1 | — | — | C20:4 (arachidonic acid) is the precursor for thromboxane-A2 and inflammatory mediator synthesis amplifying thrombotic and inflammatory responses in MI. | |
| Dihomo-gamma-linolenic acid | lipid | 1 | — | — | DGLA is an antithrombotic lipid mediator that suppresses platelet recruitment and thromboxane amplification. | |
| PTGDRPTGDR | protein | 1 | — | ◆ | PTGDR regulates prostaglandin-mediated signaling in platelets; smoking-associated variants alter thrombotic susceptibility in AMI. | |
| thromboxane prostanoid receptor alpha | protein | 1 | — | — | TPRA2 is the thromboxane-A2 G-protein-coupled receptor on platelets, whose signaling amplifies platelet recruitment and aggregation in coronary thrombosis. | |
| Thromboxane A synthase 1TBXAS1 | gene | — | — | ✦◆ | TBXAS1 encodes COX-1 product thromboxane synthase, driving platelet activation and arterial thrombosis in acute MI. |
Coagulation & thrombus formation
Coagulation / thrombus91| Molecule | Type | Conf. | Refs | Trials | Evidence | Mechanism |
|---|---|---|---|---|---|---|
| D-dimer | protein | 60 | 1 | — | D-dimer indicates active coagulation and thrombus formation during acute coronary events. | |
| FibrinogenFGA | protein | 60 | — | ◆ | Fibrinogen is the substrate for thrombin-driven fibrin polymerization forming the occlusive coronary thrombus. | |
| Plasminogen activator inhibitor-1SERPINE1 | protein | 60 | — | ✦◆ | PAI-1 inhibits fibrinolysis and promotes a prothrombotic state favoring coronary thrombus formation and persistence. | |
| Thrombin-antithrombin complex | protein | 48 | — | — | Thrombin-antithrombin complex is a marker of tissue-factor-triggered coagulation activation and thrombin generation, indicating active thrombus formation in acu | |
| Tissue FactorF3 | protein | 41 | 1 | ◆ | Tissue Factor is exposed on thrombogenic lipid-core material after plaque rupture, triggering Factor VIIa and thrombin generation. | |
| Tissue plasminogen activatorPLAT | protein | 38 | — | ✦◆ | Tissue plasminogen activator is released during coronary thrombosis and serves as a marker of fibrinolytic activity and thrombus burden in acute MI. | |
| Fibrinopeptide A | peptide | 37 | — | — | Fibrinopeptide A is released during thrombin-catalyzed fibrin polymerization, marking coagulation activation in coronary thrombosis. | |
| Prothrombin fragment 1+2F2 | protein | 29 | — | ✦◆ | F1+2 release quantifies activated prothrombin conversion, reflecting the rate of thrombin generation and coagulation activation. | |
| Thrombin | protein | 25 | 1 | — | Thrombin is generated by tissue-factor-triggered coagulation and drives fibrin polymerization and platelet activation in coronary thrombosis. | |
| Fibrinogen Beta ChainFGB | protein | 25 | — | ◆ | Fibrinogen polymerizes into fibrin scaffolding the occlusive coronary thrombus and amplifies platelet aggregation. | |
| Prothrombin Fragment 1+2 | protein | 24 | — | — | Prothrombin fragment 1+2 is released during tissue-factor-triggered coagulation, indicating thrombin generation during coronary thrombosis. | |
| Fibrin | protein | 19 | — | — | Fibrin polymerization forms the structural matrix of the occlusive coronary thrombus, with impaired fibrinolysis predicting worse outcomes. | |
| antithrombin IIISERPINC1 | protein | 17 | — | ✦◆ | Antithrombin III is consumed during thrombin-driven thrombus formation, and its depletion indicates active coagulation in acute infarction. | |
| PlasminogenPLG | protein | 16 | 1 | ✦◆ | Plasminogen activation to plasmin drives fibrin degradation and thrombus resolution in coronary occlusion. | |
| Factor VIIF7 | protein | 14 | — | ◆ | FVII activity initiates tissue-factor-mediated coagulation and fibrin-thrombus formation in MI. | |
| Factor XIF11 | protein | 12 | — | ◆ | Factor XI activation by thrombin and contact factors amplifies intrinsic coagulation in post-rupture and post-erosion thrombosis, driving coronary occlusion. | |
| Coagulation factor VIIIF8 | protein | 11 | — | ◆ | Factor VIII elevation reflects a pro-coagulative state and augments the intrinsic tenase complex, increasing thrombin generation risk. | |
| Factor VF5 | protein | 11 | — | ◆ | Factor V acts as a cofactor in the prothrombinase complex to amplify thrombin generation and drive fibrin polymerization during coronary thrombus formation. | |
| Tissue factor pathway inhibitorTFPI | protein | 11 | — | ◆ | Tissue factor pathway inhibitor antagonizes coagulation activation and thrombus formation, with inverse association to MI risk. | |
| Coagulation Factor XIIF12 | protein | 10 | — | ◆ | Factor XII activation in the contact system amplifies coagulation and contributes to thrombus formation and fibrinolytic-induced reactivation in MI. | |
| Protein CPROC | protein | 10 | — | ✦◆ | Protein C deficiency or inactivation impairs anticoagulant regulation, promoting prothrombotic thrombus formation in acute MI. | |
| Fibrin degradation products | protein | 8 | — | — | Products of plasmin-mediated fibrin degradation indicating active fibrinolysis in acute coronary thrombosis. | |
| Alpha-2-antiplasminSERPINF2 | protein | 7 | — | ◆ | Alpha-2-antiplasmin inhibits plasmin-mediated fibrin degradation; its depletion reflects active fibrinolytic turnover and indicates a hypofibrinolytic environme | |
| Kininogen-1KNG1 | protein | 7 | — | ◆ | KNG1 drives contact-triggered coagulation cascade activation and is a marker of plaque rupture and thrombus formation in Type 1 MI. | |
| Prothrombin fragment F1+2 | peptide | 7 | — | — | F1+2 is released during prothrombin activation, quantifying thrombin generation and thrombotic activity in acute MI. | |
| Thrombin-Activatable Fibrinolysis InhibitorCPB2 | protein | 7 | — | ◆ | TAFI cross-links fibrin and inhibits plasmin-mediated fibrinolysis, stabilizing the occluding thrombus in Type 1 MI. | |
| Coagulation Factor XIII A ChainF13A1 | protein | 6 | — | ◆ | Transglutaminase-catalyzing coagulation factor that stabilizes fibrin thrombus and modulates hemostatic platelet aggregation. | |
| Protease-activated receptor 1F2R | protein | 6 | — | ✦◆ | G-protein-coupled receptor activated by thrombin; drives both platelet activation and endothelial pro-inflammatory signaling during thrombosis. | |
| sphingosine-1-phosphate | lipid | 6 | — | — | Sphingosine-1-phosphate is a thrombin-downstream lipid mediator that amplifies platelet activation and coagulation responses. | |
| Coagulation Factor XF10 | protein | 5 | — | ✦◆ | Activated Factor X catalyzes prothrombin conversion to thrombin, a central step in occlusive coronary thrombus formation. | |
| Fibrinogen Gamma ChainFGG | protein | 5 | — | ◆ | Fibrinogen gamma chain polymerizes into fibrin and modulates platelet aggregation; genetic variants alter MI risk. | |
| Plasmin-α2-antiplasmin complex | complex | 5 | — | — | Plasmin-α2-antiplasmin complex indicates active fibrinolysis and proteolytic thrombus remodeling during acute coronary occlusion. | |
| uPA | protein | 5 | — | — | uPA degrades fibrin and facilitates fibrinolysis, with downregulation post-MI predicting adverse cardiac remodeling and heart failure risk. | |
| Plasma kallikreinKLKB1 | protein | 4 | — | ◆ | Kallikrein activation in the contact phase amplifies coagulation and contributes to MI risk, particularly during thrombolytic therapy-induced reactivation. | |
| Complement C3C3 | protein | 3 | — | ◆ | Central complement component driving local inflammatory amplification and thrombus-associated innate immune activation. | |
| Complement component 1q | protein | 3 | — | — | C1q initiates classical complement activation driving thrombus formation and myocardial injury in acute MI. | |
| D-dimers | protein | 3 | — | — | D-dimers reflect fibrin deposition and plasmin-mediated fibrinolysis, marking active thrombotic and fibrinolytic activity in acute coronary occlusion. | |
| Endogenous thrombin potential | other | 3 | — | — | Elevated endogenous thrombin potential indicates heightened coagulation capacity promoting thrombus formation. | |
| Inter-alpha-trypsin inhibitor heavy chain 4ITIH4 | gene | 3 | — | ◆ | Serine-protease inhibitor produced in atherosclerotic plaques and released in exosomes, predicting coronary thrombosis and acute MI. | |
| Lymphatic vessel endothelial hyaluronan receptor-1LYVE1 | protein | 3 | — | ◆ | LYVE1 marks lymphatic endothelial and macrophage infiltration in thrombus and plaque. | |
| Plasma protease C1 inhibitorSERPING1 | protein | 3 | — | ◆ | C1-inhibitor suppresses both contact-phase coagulation and complement-driven inflammation during coronary thrombus formation. | |
| Plasmin-antiplasmin complexes | protein | 3 | — | — | Plasmin-antiplasmin complexes quantify active fibrinolysis of the coronary thrombus, indicating both thrombus formation and the fibrinolytic response in acute M | |
| Soluble fibrin monomer | protein | 3 | — | — | Intermediate in fibrin polymerization indicating active coronary thrombus formation and fibrinogen consumption. | |
| Thrombin-antithrombin complexes | protein | 3 | — | — | TAT complexes quantify active thrombin generation at the site of coronary injury, marking the intensity of coagulation cascade activation in acute MI. | |
| Bradykinin | peptide | 2 | 1 | — | Kallikrein-generated vasodilatory mediator providing endothelial signaling and cardioprotection during acute thrombosis. | |
| Anticardiolipin Antibody | other | 2 | — | — | Anticardiolipin antibodies promote arterial thrombosis by enhancing coagulation and platelet activation. | |
| antiphospholipid antibodies | protein | 2 | — | — | Antiphospholipid antibodies induce a hypercoagulable state and thrombosis, causing MI in young patients. | |
| Antithrombin IIISERPENC1 | protein | 2 | — | — | Antithrombin III consumption during MI reflects thrombin and Factor Xa generation; low AT-III impairs anticoagulation and predicts thrombotic burden. | |
| Coagulation Factor IXF9 | protein | 2 | — | ◆ | Factor IX is a serine protease in the intrinsic coagulation cascade whose activity predicts venous-thromboembolism and thrombotic risk. | |
| D2-40 podoplaninPDPN | protein | 2 | — | ◆ | D2-40/podoplanin marks lymphatic endothelial involvement in coronary thrombus architecture. | |
| Heparin Cofactor IISERPIND1 | protein | 2 | — | ◆ | SERPIND1 inhibits thrombin and intrinsic tenase, regulating coagulation amplification during acute MI. | |
| Histidine-Rich GlycoproteinHRG | protein | 2 | — | ◆ | Histidine-rich glycoprotein regulates coagulation and platelet adhesion, influencing thrombus formation in Type 1 MI. | |
| miR-197-5p | rna | 2 | — | — | miR-197-5p dysregulation in unstable angina and STEMI associates with altered coagulation and platelet activation cascades. | |
| miR-361-5p | rna | 2 | — | — | miR-361-5p dysregulation in acute MI associates with altered coagulation cascade activation and adverse major events. | |
| Plasmin-inhibitor complex | complex | 2 | — | — | Plasmin-inhibitor complex marks active fibrinolysis and thrombus remodeling in myocardial infarction. | |
| Vascular endothelial growth factor receptor 3FLT4 | protein | 2 | — | ◆ | VEGFR3 expression marks lymphatic endothelial cells infiltrating coronary thrombus. | |
| Activated Protein CPC | protein | 1 | — | ◆ | Activated Protein C generation marks thrombin-driven anticoagulant feedback and reflects acute coagulation activation during MI. | |
| AGBL1AGBL1 | protein | 1 | — | — | AGBL1 variants influence activated partial thromboplastin time, a coagulation trait linked to CAD thrombotic risk. | |
| Alpha-2 macroglobulinA2M | protein | 1 | — | ◆ | Broad-spectrum protease inhibitor involved in thrombin inhibition and fibrinolytic regulation during acute thrombosis. | |
| Annexin V-binding small microparticles | complex | 1 | — | — | Annexin V-binding microparticles provide a procoagulant surface promoting thrombus formation in acute coronary syndromes. | |
| Anti-β2-glycoprotein I antibodies | protein | 1 | — | — | Anti-β2-glycoprotein I antibodies promote a prothrombotic state through phospholipid-dependent coagulation activation. | |
| APC-PCI | protein | 1 | — | — | APC-PCI (activated protein C-protein C inhibitor complex) reflects ongoing thrombin generation and coagulation amplification during coronary thrombosis. | |
| C4b-binding protein alpha-chainC4BPA | protein | 1 | — | ◆ | C4b-binding protein modulates complement activation and anticoagulation during coronary thrombus formation. | |
| CD144+ tissue-factor+ microparticles | complex | 1 | — | — | CD144+TF+ microparticles from activated endothelium carry tissue factor to trigger thrombin generation and fibrin deposition. | |
| Cross-linked fibrin degradation products | protein | 1 | — | — | Cross-linked fibrin degradation products reflect active thrombus formation and fibrinolytic activity, indicating thrombus burden and complexity in MI. | |
| Crosslinked fibrin degradation products | protein | 1 | — | — | Crosslinked fibrin degradation products reflect Factor XIII-stabilized thrombus formation and endogenous fibrinolytic activation. | |
| Erythrocyte Membrane Particles | complex | 1 | — | — | Erythrocyte-derived microparticles serve as markers of vascular injury and contribute to coagulation amplification in acute coronary syndrome. | |
| Fibrin degradation product | peptide | 1 | — | — | Fibrin degradation products indicate active fibrinolytic remodeling and coagulation turnover during acute MI. | |
| Fibrin fragment beta 15-42 | peptide | 1 | — | — | Fibrin-derived peptide released during fibrin polymerization and plasmin-mediated degradation in acute thrombus. | |
| Fibrin/fibrinogen degradation products | protein | 1 | — | — | Fibrin/fibrinogen degradation products reflect active thrombus formation and plasmin-driven fibrinolysis within the occlusive thrombus. | |
| Fibrinogen B-beta 15-42 peptide | peptide | 1 | — | — | Fibrinogen B-beta 15-42 peptide is a fibrin-specific breakdown product marking active fibrinolysis and thrombus remodeling. | |
| Fibrinogen/fibrin fragment E | peptide | 1 | — | — | Fragment E released during fibrin degradation reflects active coagulation and fibrinolytic turnover in the coronary thrombus. | |
| Fragment D neoantigen | peptide | 1 | — | — | Neoepitope released during fibrinolytic degradation of cross-linked fibrin in coronary thrombus. | |
| Fragment E | peptide | 1 | — | — | Fibrin degradation product marking thrombin-driven coagulation and fibrinolytic turnover in acute coronary thrombosis. | |
| Fragment E neoantigen | peptide | 1 | — | — | Neoepitope released during fibrinolytic degradation indicating active thrombus formation and fibrin turnover. | |
| FX-06 | peptide | 1 | — | — | FX-06 is a fibrin-derived peptide that mitigates ischemia-reperfusion injury following coronary thrombus resolution. | |
| Homocysteine thiolactone | metabolite | 1 | — | — | Homocysteine thiolactone modulates fibrin structure and plasmin-mediated lysis, influencing thrombus stability and fibrinolytic resistance in acute MI. | |
| Lupus Anticoagulant | other | 1 | — | — | Lupus anticoagulant promotes coronary thrombosis through tissue-factor and coagulation pathway activation. | |
| Myosin | protein | 1 | — | — | Myosin-driven actin sliding powers platelet contraction and thrombus compaction, enabling the transition from loose plug to stable occlusive clot. | |
| P-selectin+ tissue-factor+ microparticles | complex | 1 | — | — | CD62P+TF+ microparticles simultaneously mark platelet activation and deliver tissue factor to amplify thrombus formation. | |
| PAI-2SERPINB2 | protein | 1 | — | ◆ | PAI-2 regulates fibrinolysis by inhibiting tissue plasminogen activator and urokinase, modulating thrombus stabilization and resolution. | |
| Plasmin-alpha2-plasmin inhibitor complex | complex | 1 | — | — | Plasmin-alpha2-plasmin inhibitor complex quantifies fibrinolysis and thrombus burden in acute coronary thrombosis. | |
| Protein C activation peptide | peptide | 1 | — | — | Peptide released during activated Protein C generation, marking endogenous anticoagulant pathway engagement. | |
| Protein ZPROZ | gene | 1 | — | ◆ | Protein Z is a vitamin K-dependent anticoagulant that influences coagulation balance and thrombotic risk. | |
| Red blood cell-derived microparticles | complex | 1 | — | — | RBC-derived microparticles marking thrombotic activation and hemolysis during acute coronary occlusion. | |
| Thrombin peak (generation) | protein | 1 | — | — | Thrombin peak represents the maximum rate of thrombin generation, reflecting coagulation cascade activation and fibrin formation intensity. | |
| Tissue Plasminogen Activator / Plasminogen Activator Inhibitor-1 Ratio | complex | 1 | — | — | The tPA/PAI-1 ratio quantifies net fibrinolytic activity; low ratio signals impaired thrombus lysis and predicts worse reperfusion in acute MI. | |
| tPA/PAI-1 complex | complex | 1 | — | — | tPA/PAI-1 complex imbalance (excess PAI-1) suppresses fibrinolysis and promotes thrombus persistence in coronary occlusion. | |
| Tropomyosin | protein | 1 | — | — | Tropomyosin stabilizes actin filaments in the platelet cytoskeleton, reinforcing thrombus structural organization and mechanical integrity. | |
| ABO Histo-Blood GroupABO | gene | — | — | ✦ | Blood-group determinant modulating von Willebrand factor and clotting-factor levels. | |
| gamma-glutamyl carboxylaseGGCX | gene | — | — | ✦◆ | Catalyzes vitamin K-dependent carboxylation of coagulation factors (II, VII, IX, X) and vascular Gla proteins (MGP, osteocalcin); deficiency impairs thrombus re |
Myocardial injury (shared endpoint)
Myocardial injury254| Molecule | Type | Conf. | Refs | Trials | Evidence | Mechanism |
|---|---|---|---|---|---|---|
| Cardiac troponin ITNNI3 | protein | 60 | 2 | ✦◆ | Cardiac troponin I is released from damaged cardiomyocytes following myocardial ischemia and necrosis and is the gold-standard biomarker for acute MI diagnosis, | |
| CK-MBCKM | protein | 51 | 1 | ◆ | CK-MB is a cardiac enzyme released following myocardial necrosis and serves as a diagnostic and prognostic biomarker of infarct size and adverse outcomes in acu | |
| Troponin TTNNT2 | protein | 47 | 6 | ✦◆ | Cardiac troponin T is released from damaged cardiomyocytes following myocardial ischemia and necrosis and is the primary biomarker for acute MI diagnosis, progn | |
| H-FABPFABP3 | protein | 18 | 1 | ◆ | H-FABP is released early from myocardial ischemia and necrosis, serving as an early biomarker of cardiomyocyte injury in acute MI. | |
| CopeptinAVP | peptide | 14 | 5 | ✦◆ | Copeptin is released in response to myocardial ischemia and necrosis, providing early detection of acute coronary syndrome alongside cardiomyocyte injury. | |
| MyoglobinMB | protein | 14 | — | ✦◆ | Myoglobin released from ischemic cardiomyocytes serves as an early biomarker of myocardial infarction and necrotic injury. | |
| Transforming Growth Factor-BetaTGFB1 | protein | 12 | — | ✦◆ | TGF-β drives myocardial fibrosis and remodeling following ischemic injury and modulates plaque inflammation via foam cell formation. | |
| lactate dehydrogenase | protein | 9 | — | — | LDH is released from ischemic and necrotic myocardium during acute infarction, indicating cardiomyocyte death. | |
| acylcarnitines | metabolite | 8 | — | — | Acylcarnitines accumulate during ischemic myocardial injury reflecting impaired fatty-acid oxidation and energy metabolism. | |
| Creatine Kinase | protein | 8 | — | — | CK is released from infarcting myocardium upon cardiomyocyte rupture and necrosis, serving as an early marker of myocardial injury in acute MI. | |
| Creatine kinase-MB | protein | 7 | — | — | Creatine kinase-MB is released from necrotic cardiomyocytes, quantifying the extent of myocardial necrosis in acute myocardial infarction. | |
| Glutamine | metabolite | 7 | — | — | Dysregulated glutamine metabolism in acute myocardial injury reflects impaired amino-acid homeostasis and cardiomyocyte energetics. | |
| Ischemia-modified albuminALB | protein | 7 | — | ✦◆ | Ischemia-modified albumin (IMA) is an early albumin modification arising from myocardial ischemia that serves as a sensitive early ACS biomarker preceding tropo | |
| miR-1 | rna | 6 | — | — | miR-1 is released from ischemic myocardium and dysregulated in MI; elevated levels indicate cardiomyocyte injury and arrhythmia risk. | |
| miR-133a | rna | 6 | — | — | miR-133a is released into circulation upon myocardial necrosis and endothelial injury, serving as a sensitive biomarker for AMI detection. | |
| miR-499 | rna | 6 | — | — | miR-499, cardiac-specific microRNA, is released early in myocardial ischemia and necrosis; elevated levels indicate cardiomyocyte damage and endothelial injury. | |
| Succinate | metabolite | 6 | — | — | Succinate accumulates during myocardial ischemia and generates ROS upon reperfusion, marking cardiomyocyte injury and ischemia-reperfusion damage in STEMI. | |
| Cardiac troponin | protein | 4 | 7 | — | Cardiac troponin is released from damaged cardiomyocytes upon ischemic necrosis, serving as the diagnostic standard for myocardial infarction. | |
| BaxBAX | protein | 4 | — | ◆ | Bax activation drives mitochondrial outer-membrane permeabilization and cardiomyocyte apoptosis during myocardial ischemic injury. | |
| Bcl-2BCL2 | protein | 4 | — | ◆ | Bcl-2 overexpression suppresses Bax-mediated mitochondrial apoptosis and protects cardiomyocytes against ischemic necrosis in myocardial infarction. | |
| Cardiac Myosin-Binding Protein CMYBPC3 | protein | 4 | — | — | Cardiac myosin-binding protein C is released into circulation upon cardiomyocyte necrosis, marking myocardial injury in acute MI. | |
| Caspase-3CASP3 | protein | 4 | — | ◆ | Caspase-3 activation drives cardiomyocyte apoptosis during myocardial ischemia and marks programmed cell death in infarction. | |
| Kynurenic acid | metabolite | 4 | — | — | Kynurenic acid, derived from tryptophan metabolism, is downregulated in acute coronary syndromes; reduced levels reflect metabolic dysregulation and impaired ca | |
| Taurine | metabolite | 4 | — | — | Taurine is a conditionally essential amino acid that provides cardioprotection during myocardial ischemia-reperfusion and supports long-term post-MI recovery. | |
| Tyrosine 3-Monooxygenase/Tryptophan 5-Monooxygenase Activation Protein ZetaYWHAZ | protein | 4 | — | ◆ | YWHAZ (14-3-3-zeta) is a cardioprotective adaptor protein whose downregulation in acute MI reflects early cardiomyocyte injury and ischemic stress. | |
| creatine | metabolite | 3 | — | — | Creatine dysregulation reflects impaired myocardial energetics in acute coronary syndrome and recovery, marking cardiomyocyte ischemic injury and metabolic rest | |
| Cytochrome cCYCS | protein | 3 | — | ◆ | Mitochondrial-release apoptosis and ferroptosis marker indicating programmed cardiomyocyte death during acute ischemic injury. | |
| FasFAS | protein | 3 | — | ◆ | Fas mediates apoptosis in both cardiomyocytes and endothelial cells, contributing to ischemic injury and vascular dysfunction. | |
| Glutathione | metabolite | 3 | — | — | Glutathione depletion during myocardial ischemia impairs antioxidant defense and amplifies cardiomyocyte injury. | |
| Inosine | metabolite | 3 | — | — | Nucleoside byproduct of ATP degradation during myocardial ischemia, signaling rapid cardiomyocyte energy stress. | |
| Lactate dehydrogenaseLDHA | protein | 3 | — | ◆ | Lactate dehydrogenase released from ischemic cardiomyocytes and endothelial cells serves as an acute myocardial injury and tissue-damage marker. | |
| Lysine | metabolite | 3 | — | — | Essential amino acid dysregulation in acute MI reflecting altered cardiac protein turnover and ischemic metabolic shift. | |
| miR-208 | rna | 3 | — | — | miR-208 is a cardiac-specific microRNA released early in myocardial infarction that serves as a sensitive indicator of cardiomyocyte damage. | |
| Myo-inositol | metabolite | 3 | — | — | Inositol metabolism perturbation reflects myocardial ischemic stress and membrane phospholipid turnover during cardiac injury. | |
| PeriostinPOSTN | protein | 3 | — | ◆ | POSTN is expressed by infarct-associated fibroblasts and macrophages, driving extracellular matrix remodeling and scar formation after myocardial necrosis. | |
| Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-AlphaPPARGC1A | protein | 3 | — | ◆ | PGC-1α protects cardiomyocytes through mitochondrial biogenesis and oxidative stress reduction. | |
| TNF-Related Apoptosis-Inducing Ligand Receptor 2TNFRSF10B | protein | 3 | — | ◆ | TRAIL-R2 mediates apoptotic pathways in cardiomyocytes and immune cells, predicting MI incidence and post-MI mortality. | |
| c-KitKIT | protein | 2 | 1 | ◆ | c-Kit+ cardiac progenitor cells mobilize in response to myocardial necrosis, contributing to post-MI remodeling and repair. | |
| 5-Hydroxy-L-tryptophan | metabolite | 2 | — | — | Tryptophan metabolite upregulated in myocardial necrosis, reflecting cardiomyocyte damage and metabolic stress. | |
| Acetylglycine | metabolite | 2 | — | — | Acetylglycine elevation identifies acute myocardial infarction and stratifies cardiac prognosis in acute coronary syndromes. | |
| cfDNA | other | 2 | — | — | Cell-free DNA released from necrotic myocardium, reflecting infarct size and severity in acute myocardial infarction. | |
| Dual specificity phosphatase 1DUSP1 | gene | 2 | — | ◆ | DUSP1 dysregulation in acute MI reflects cardiomyocyte ferroptosis and ischemic death signaling. | |
| epoxyeicosatrienoic acids | lipid | 2 | — | — | Epoxyeicosatrienoic acids are cardioprotective lipid mediators derived from arachidonic acid that promote myocardial repair and inflammation resolution. | |
| Glutamate | metabolite | 2 | — | — | Excitatory amino-acid dysregulation impairs cardiovascular homoeostasis and contributes to ischemic myocardial injury. | |
| Glutamic oxaloacetic transaminase 1GOT1 | protein | 2 | — | ◆ | Cytoplasmic transaminase released from cardiomyocyte necrosis reflecting ischemic myocardial injury. | |
| Glutamic oxaloacetic transaminase 2GOT2 | protein | 2 | — | ✦◆ | Mitochondrial transaminase release during myocardial necrosis indicating cardiac cell death in acute MI. | |
| Glutathione peroxidase 3GPX3 | gene | 2 | — | ◆ | GPX3 mitigates oxidative stress during myocardial ischemia and lipoprotein oxidation. | |
| Heat shock protein A8HSPA8 | protein | 2 | — | ◆ | HSPA8 regulates protein quality control and ferroptotic cardiomyocyte death in MIRI. | |
| histidine | metabolite | 2 | — | — | Histidine dysregulation associates with myocardial injury severity and acute-phase metabolic derangement in MI progression. | |
| JDP2 transcription factorJDP2 | gene | 2 | — | — | JDP2 regulates ferroptotic cardiomyocyte injury and post-MI immune tolerance programs. | |
| Lactate Dehydrogenase BLDHB | protein | 2 | — | ◆ | Lactate dehydrogenase B is released from damaged cardiomyocytes during ischemic necrosis, serving as a biomarker of myocardial infarction. | |
| Linoleoyl carnitine (C18:2) | metabolite | 2 | — | — | Ischemia-induced mitochondrial dysfunction generates acylcarnitine biomarkers of myocardial energy depletion. | |
| LPC (18:2) | lipid | 2 | — | — | Decreased LPC (18:2) content post-MI reflects myocardial injury, phospholipase-A2 activation, and inflammatory lipid mediator generation. | |
| Malate Dehydrogenase | protein | 2 | — | — | Malate dehydrogenase is a mitochondrial enzyme whose reduced activity and release during myocardial infarction reflects cardiomyocyte necrosis and bioenergetic | |
| Mannitol | metabolite | 2 | — | — | A polyol metabolite reflecting myocardial metabolic stress and serving as a prognostic marker in acute coronary syndrome. | |
| microRNA-19a | rna | 2 | — | — | miR-19a is released during myocardial ischemia and necrosis, serving as an early circulating biomarker of acute MI. | |
| miR-183-5p | rna | 2 | — | — | miR-183-5p is elevated in NSTEMI and detects acute myocardial injury with diagnostic utility for acute coronary syndromes. | |
| miR-208b | rna | 2 | — | — | miR-208b dysregulation marks myocardial ischemic injury and ischemia-reperfusion stress in acute MI. | |
| miR-23a-3p | rna | 2 | — | — | miR-23a-3p is dysregulated during acute MI, modulating cardiomyocyte oxidative stress and predicting post-MI heart failure. | |
| miR-484 | rna | 2 | — | — | miR-484 is acutely elevated during acute myocardial infarction and serves as a diagnostic biomarker for acute coronary events. | |
| Peptidylprolyl Isomerase A (Cyclophilin A)PPIA | protein | 2 | — | ✦◆ | PPIA downregulation in acute MI reflects disruption of intracellular protein folding and cellular stress in ischemic myocardium. | |
| Phosphatidic acid | lipid | 2 | — | — | Phospholipid dysregulated in myocardial ischemia-reperfusion injury and cardiomyocyte damage. | |
| Serine | metabolite | 2 | — | — | An amino acid employed in metabolite-ratio diagnostics for acute myocardial necrosis in STEMI. | |
| SLC22A2 (OCT2)SLC22A2 | protein | 2 | — | ✦◆ | SLC22A2 genetic variation modulates cardiomyocyte acylcarnitine uptake and reperfusion-injury sensitivity. | |
| Sorbitol | metabolite | 2 | — | — | A polyol reflecting myocardial metabolic perturbation and osmotic stress, used in prognostic stratification of acute coronary syndrome risk. | |
| Triosephosphate Isomerase 1TPI1 | protein | 2 | — | ◆ | TPI1 release marks cardiomyocyte damage during acute ischemia and ischemia-reperfusion injury in MI. | |
| Tumor Protein p53TP53 | protein | 2 | — | ◆ | p53 promotes ferritinophagy-driven iron metabolism during myocardial ischemia and contributes to cardiomyocyte death and plaque instability. | |
| xanthosine | metabolite | 2 | — | — | Xanthosine alleviates myocardial ischemia-reperfusion injury and ferroptosis, protecting cardiomyocytes through energy metabolism restoration. | |
| Carnitine | metabolite | 1 | 1 | — | Carnitine concentration changes reflect myocardial fatty-acid oxidation and energetic stress during acute myocardial infarction. | |
| Caspase | protein | 1 | 1 | — | Caspase activation executes apoptosis and cleaves contractile proteins in cardiomyocytes during ischemic injury and reperfusion-mediated cell death. | |
| 11-Retinol | metabolite | 1 | — | — | Vitamin-A metabolite biomarker diagnostic of acute myocardial infarction via metabolic disruption in ischemia. | |
| 2-Hydroxy-6-aminopurine | metabolite | 1 | — | — | 2-Hydroxy-6-aminopurine is a nucleotide-derived metabolite elevated in acute myocardial injury. | |
| 2,5-Dihydroxybenzenesulfonic acid | metabolite | 1 | — | — | Differential metabolite accumulating in post-MI cardiac dysfunction and ischemic injury. | |
| 3-OH-kynurenine | metabolite | 1 | — | — | A kynurenine-pathway metabolite reflecting tryptophan catabolism and ischemic myocardial injury in Type 1 MI. | |
| Actin Binding LIM Protein 1ABLIM1 | gene | 1 | — | — | ABLIM1 phosphorylation reflects cardiomyocyte cytoskeletal remodeling and stress response in MI. | |
| Actin, Alpha 1ACTA1 | gene | 1 | — | ◆ | ACTA1 upregulation reflects myocardial structural remodeling and cardiomyocyte injury during acute MI. | |
| Acyl-CoA Dehydrogenase Medium ChainACADM | gene | 1 | — | ◆ | ACADM variants reduce fatty-acid β-oxidation capacity, compromising ATP supply and increasing cardiomyocyte ischemic injury during acute MI. | |
| Adducin 3ADD3 | protein | 1 | — | ◆ | ADD3 maintains cardiomyocyte sarcomeric integrity and contractility, with expression changes predicting post-infarction ventricular remodeling. | |
| Alpha-galactosidaseGLA | gene | 1 | — | ◆ | Alpha-galactosidase gene upregulation driving sphingolipid catabolism in ischemia-reperfusion injury. | |
| Ankyrin repeat domain-containing protein 1ANKRD1 | gene | 1 | — | — | ANKRD1 is expressed during cardiomyocyte stress and post-ischemic remodeling. | |
| Anthranilic acid | metabolite | 1 | — | — | A tryptophan-derived metabolite elevated in STEMI that reflects kynurenine-pathway activation and myocardial ischemic injury. | |
| ApoJ-GlycAPOJ | lipoprotein | 1 | — | — | Clusterin (ApoJ) glycoprotein variant released during myocardial ischemia and endothelial injury. | |
| Apolipoprotein L1APOL1 | protein | 1 | — | ◆ | Apolipoprotein L1 phosphorylation accompanies acute myocardial injury and inversely correlates with troponin release. | |
| Aquaporin-1AQP1 | gene | 1 | — | ◆ | AQP1 controls myocardial water transport and edema formation during ischemic-reperfusion injury after myocardial infarction. | |
| Aspartic acid | metabolite | 1 | — | — | An amino acid component of diagnostic metabolite-ratio panels for distinguishing acute myocardial necrosis. | |
| ATP synthase subunit dATP5H | gene | 1 | — | — | ATP5H dysfunction triggers ferroptotic cardiomyocyte death during myocardial ischemia-reperfusion injury after coronary occlusion. | |
| ATPase Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase 2ATP2A2 | gene | 1 | — | ✦◆ | ATP2A2 phosphorylation dysregulates calcium homeostasis in ischemic cardiomyocytes following Type 1 MI. | |
| BCAT1BCAT1 | protein | 1 | — | ◆ | BCAT1 (branched-chain amino-acid aminotransferase 1) mediates OXE-R-driven cardioprotection, reducing myocardial ischemic injury in Type 1 MI. | |
| BCL2-Associated Athanogene 3BAG3 | protein | 1 | — | — | BAG3 reflects cardiomyocyte ischemic stress and proteostasis dysfunction during myocardial injury and post-MI remodeling. | |
| BCL2L1BCL2L1 | gene | 1 | — | ◆ | BCL2L1 (Bcl-xL) is an anti-apoptotic gene whose downregulation via miR-133a promotes cardiomyocyte apoptosis in ischemic injury. | |
| BCL2L13BCL2L13 | protein | 1 | — | ◆ | BCL2L13 suppression by miR-96-5p promotes cardiomyocyte apoptosis during myocardial ischemia and infarction. | |
| Bromodomain-containing protein 2BRD2 | protein | 1 | — | ◆ | BRD2 suppresses ischemia-reperfusion injury and cardiomyocyte death, reducing myocardial infarction severity. | |
| C-terminal agrin fragment | peptide | 1 | — | — | A proteolytic agrin fragment that marks myocardial necrosis and predicts post-infarction acute kidney injury through systemic inflammatory and ischemic stress p | |
| C14:1-OH (14:1 hydroxy-acylcarnitine) | metabolite | 1 | — | — | C14:1-OH accumulates during myocardial ischemia due to impaired fatty-acid β-oxidation and reflects cardiomyocyte metabolic stress. | |
| Calpain | protein | 1 | — | — | Calpain mediates calcium-dependent proteolysis of cardiomyocyte structural and contractile proteins during acute myocardial ischemia and necrosis. | |
| Cardiac Troponin T/ITNNT2/TNNI3 | protein | 1 | — | — | Cardiac troponins released from injured cardiomyocytes are the diagnostic standard for myocardial infarction detection and risk stratification. | |
| Cardiac troponins | protein | 1 | — | — | Cardiac troponins (I, T, C) are released upon cardiomyocyte necrosis and are the definitive biomarker for myocardial injury in acute myocardial infarction. | |
| Caspase-8CASP8 | protein | 1 | — | ◆ | Caspase-8 is released during ischemic cardiomyocyte apoptosis and serves as an early myocardial-injury marker distinct from troponin. | |
| Chromobox Protein Homolog 3CBX3 | gene | 1 | — | — | CBX3 phosphorylation indicates nuclear/chromatin stress response in ischemic cardiomyocytes. | |
| circMap4k2 | rna | 1 | — | — | CircMap4k2 regulates cardiac repair processes and reduces myocardial remodeling following ischemic injury. | |
| circPRDM5 | rna | 1 | — | — | circPRDM5 release during acute MI indicates cardiomyocyte necrosis and ischemic injury extent. | |
| cis-4-hydroxy-D-proline | metabolite | 1 | — | — | STEMI-associated metabolite marker of altered amino-acid catabolism during acute myocardial injury. | |
| Complement C1q subcomponent subunit AC1QA | protein | 1 | — | ◆ | Complement C1q is activated post-infarction by exposure of myocardial autoantigens and contributes to inflammatory myocardial injury. | |
| CPT1ACPT1A | protein | 1 | — | ◆ | CPT1A inhibition during reperfusion impairs myocardial energy metabolism and elevates acylcarnitine markers. | |
| CRIPTOCRIPTO | protein | 1 | — | ◆ | CRIPTO is a cardiac developmental factor upregulated as a myocardial injury indicator in acute MI. | |
| Cut-Like Homeobox 1CUX1 | protein | 1 | — | — | CUX1 regulates cardiomyocyte-stress responses and post-infarction remodeling, predicting adverse cardiac outcomes. | |
| Cystatin BCSTB | protein | 1 | — | ◆ | Cystatin B is a protease inhibitor released during myocardial ischemia and injury, with levels inversely correlating to left ventricular function. | |
| Cysteic acid | metabolite | 1 | — | — | Cysteic acid elevation indicates cysteine oxidation and myocardial oxidative stress during acute myocardial infarction. | |
| Cysteine and glycine-rich protein 3CSRP3 | protein | 1 | — | — | CSRP3 is a cardiac-restricted protein released upon cardiomyocyte injury and serves as an early MI damage marker. | |
| Cytokine receptor-like factor 1CRLF1 | protein | 1 | — | ◆ | CRLF1 is a post-MI cardiac fibroblast-derived factor that modulates myocardial repair and inflammatory response. | |
| D-aspartic acid | metabolite | 1 | — | — | NSTEMI-associated metabolite reflecting altered amino-acid metabolism in acute myocardial stress. | |
| Death-Associated Protein Kinase 3DAPK3 | gene | 1 | — | ◆ | DAPK3 promotes cardiomyocyte apoptosis and death during myocardial ischemia, exacerbating injury in Type 1 MI. | |
| Decanoylcarnitine | metabolite | 1 | — | — | Decanoylcarnitine accumulation reflects impaired mitochondrial fatty-acid oxidation during acute myocardial infarction. | |
| Dicarboxylacylcarnitines | metabolite | 1 | — | — | Dicarboxylacylcarnitine accumulation reflects impaired mitochondrial fatty-acid oxidation and energetic crisis in myocardial injury. | |
| Dickkopf-4DKK4 | protein | 1 | — | ◆ | DKK4 is a Wnt pathway inhibitor associated with myocardial injury and post-MI remodeling. | |
| Digalactosylceramide | lipid | 1 | — | — | Sphingolipid depleted in myocardial ischemia-reperfusion injury and lipid remodeling. | |
| DNA-damage-inducible transcript 4DDIT4 | gene | 1 | — | — | DDIT4 integrates ischemic stress signals and ferroptotic pathways, predicting post-MI cardiac dysfunction. | |
| Drp1DNM1L | protein | 1 | — | ◆ | Drp1 (DNM1L) drives mitochondrial fission during cardiomyocyte ischemia and necrosis in acute myocardial infarction. | |
| DysferlinDYSF | protein | 1 | — | ◆ | Dysferlin dysfunction impairs cardiomyocyte membrane integrity during ischemic injury, exacerbating myocardial damage. | |
| EIF2AK3EIF2AK3 | gene | 1 | — | ◆ | EIF2AK3 activation by mitochondrial dysfunction contributes to cardiomyocyte necrosis during myocardial ischemia. | |
| Enoyl-CoA Isomerase 2ECI2 | gene | 1 | — | ◆ | ECI2 deficiency impairs mitochondrial fatty-acid oxidation, reducing ATP production and increasing cardiomyocyte vulnerability to ischemic injury. | |
| ENST00000416860.2 | rna | 1 | — | — | Circulating lncRNA dysregulated in acute myocardial infarction; precise mechanistic role in atherothrombotic cascade undefined. | |
| Eukaryotic Translation Initiation Factor 4BEIF4B | gene | 1 | — | ◆ | EIF4B phosphorylation indicates translational stress response in ischemic cardiomyocytes. | |
| FBXO32FBXO32 | gene | 1 | — | — | FBXO32 (atrogin-1) is a muscle-specific E3 ligase elevated during cardiomyocyte damage and proteolysis in acute myocardial infarction. | |
| FENDRRFENDRR | rna | 1 | — | — | FENDRR regulates ferritinophagy in myocardial ischemia, controlling iron-mediated oxidative stress and cardiomyocyte injury. | |
| Ferulic acid | metabolite | 1 | — | — | Ferulic acid reflects oxidative stress and phenolic metabolism dysregulation during acute myocardial infarction. | |
| Free fatty acid (15:1) | lipid | 1 | — | — | Free fatty acid (15:1) elevation discriminates atherothrombotic MI from Type 2 MI, marking ischemic lipid catabolism. | |
| Galactosylceramide | lipid | 1 | — | — | Sphingolipid accumulating in myocardial ischemia-reperfusion injury and cardiomyocyte death. | |
| Glucocorticoid steroid metabolites | metabolite | 1 | — | — | Stress-induced glucocorticoid metabolites reflect acute systemic perturbation and hemodynamic stress during Type 1 MI. | |
| Glucose transporter 1SLC2A1 | gene | 1 | — | ◆ | GLUT1 upregulation facilitates myocardial glucose uptake during ischemia-reperfusion injury. | |
| Glucose transporter 4SLC2A4 | gene | 1 | — | ◆ | GLUT4 dysregulation impairs myocardial glucose handling and energetics during ischemia-reperfusion. | |
| Glutarylglycine | metabolite | 1 | — | — | Glutarylglycine elevation identifies acute myocardial infarction and discriminates cardiac-risk phenotypes in acute coronary syndromes. | |
| Glycogen Phosphorylase BBPYGB | protein | 1 | — | ◆ | PYGB (glycogen phosphorylase BB) is released during myocardial ischemia and necrosis, marking acute cardiomyocyte injury. | |
| Granzyme KGZMK | gene | 1 | — | ◆ | GZMK is a cytotoxic T cell effector molecule contributing to post-MI cardiomyocyte damage. | |
| Guanidineacetic acid | metabolite | 1 | — | — | Guanidineacetic acid is a creatine-pathway metabolite elevated during myocardial ischemia and energetic derangement. | |
| HECW2HECW2 | gene | 1 | — | — | HECW2 is elevated in acute coronary syndrome but its specific role in atherothrombotic pathophysiology remains to be defined. | |
| hsa-miR-186-5p | rna | 1 | — | — | A circulating microRNA dysregulated in myocardial infarction with utility in early disease detection. | |
| hsa-miR-21-3p | rna | 1 | — | — | A microRNA dysregulated in myocardial infarction that modulates inflammatory and apoptotic pathways contributing to ischemic cardiomyocyte injury. | |
| hsa-miR-296-5p | rna | 1 | — | — | A circulating microRNA dysregulated in coronary artery disease and myocardial infarction that modulates angiogenic and vascular responses. | |
| hsa-miR-29a-5p | rna | 1 | — | — | A circulating microRNA dysregulated in coronary artery disease and myocardial infarction that regulates fibrotic and inflammatory remodeling. | |
| hsa-miR-32-3p | rna | 1 | — | — | A circulating microRNA dysregulated in myocardial infarction with utility in early disease detection. | |
| HtrA2/Omi protease | protein | 1 | — | — | A mitochondrial serine protease released into circulation during ischemic cardiomyocyte apoptosis, marking myocardial necrosis in acute ST-elevation infarction. | |
| Hydroxynicotinic acid | metabolite | 1 | — | — | Nicotinic acid metabolite depletion in myocardial injury marks impaired NAD+ cycling and cardiomyocyte bioenergetic stress. | |
| Hydroxyphenyllactic acid | metabolite | 1 | — | — | Hydroxyphenyllactic acid elevation reflects myocardial hypoxia and metabolic disturbance during acute infarction. | |
| Hypotaurine | metabolite | 1 | — | — | Hypotaurine provides antioxidant and cytoprotective functions during myocardial ischemia-reperfusion, attenuating cardiomyocyte injury. | |
| Hypoxanthine | metabolite | 1 | — | — | Hypoxanthine is an early metabolite marker of myocardial ischemic injury from accelerated purine degradation. | |
| Ischaemia-modified albumin | protein | 1 | — | — | Ischaemia-modified albumin accumulates during acute myocardial ischaemia as a product of hypoxia-induced and oxidative-stress-dependent albumin metal-binding al | |
| Isocitric acid | metabolite | 1 | — | — | Isocitric acid downregulation in ACS reflects impaired aerobic metabolism and myocardial energy depletion during acute ischemia. | |
| KBTBD10KBTBD10 | gene | 1 | — | — | KBTBD10 is a cardiac/muscle-specific ubiquitin ligase elevated during myocardial ischemic injury and proteolytic remodeling in acute myocardial infarction. | |
| Krüppel-like factor 5KLF5 | gene | 1 | — | ◆ | KLF5 activation aggravates ischemia-reperfusion injury and cardiomyocyte apoptosis during MI. | |
| L-Acetylcarnitine | metabolite | 1 | — | — | L-Acetylcarnitine dysregulation reflects impaired myocardial fatty-acid oxidation and energy depletion during STEMI. | |
| L-arachidoyl carnitine | metabolite | 1 | — | — | L-arachidoyl carnitine accumulates in myocardial necrosis, serving as an early ischemia and cardiomyocyte damage marker. | |
| L-Aspartic acid | metabolite | 1 | — | — | L-Aspartic acid elevation reflects myocardial necrosis and amino acid loss during acute infarction. | |
| L-Glutamate | metabolite | 1 | — | — | Glutamate depletion in acute myocarditis marks cardiomyocyte dysfunction and altered mitochondrial metabolism. | |
| L-Homocysteine sulfinic acid | metabolite | 1 | — | — | L-Homocysteine sulfinic acid elevation reflects oxidative stress and myocardial ischaemia during acute myocardial infarction. | |
| Lauroylcarnitine | metabolite | 1 | — | — | Lauroylcarnitine accumulation reflects impaired mitochondrial fatty-acid oxidation during acute myocardial infarction. | |
| let-7g-5p | rna | 1 | — | — | let-7g-5p distinguishes unstable angina from overt myocardial infarction through differential expression patterns in ischemic injury. | |
| let-7i-5pMIRLET7I | rna | 1 | — | — | Circulating let-7i-5p serves as an early diagnostic marker of myocardial ischemia in STEMI. | |
| LIN28ALIN28A | protein | 1 | — | — | LIN28A promotes cardiomyocyte survival and metabolic adaptation by upregulating PDK1-mediated glycolysis post-infarction. | |
| Linoleoyl carnitine (C18:2-carnitine) | metabolite | 1 | — | — | Ischemia-reperfusion impairs mitochondrial fatty-acid oxidation, elevating long-chain acylcarnitines as injury markers. | |
| Long-chain acylcarnitine (16:1) | metabolite | 1 | — | — | Elevated LCAC reflects impaired myocardial fatty-acid β-oxidation during reperfusion ischemia. | |
| LPC (18:0) | lipid | 1 | — | — | Decreased LPC (18:0) content post-MI reflects phospholipid catabolism linked to myocardial injury and inflammatory response. | |
| LPC (18:3) | lipid | 1 | — | — | Decreased LPC (18:3) content post-MI reflects polyunsaturated-phospholipid catabolism and myocardial injury. | |
| LPC (20:0) | lipid | 1 | — | — | Decreased LPC (20:0) content post-MI reflects phospholipid catabolism and myocardial dysfunction severity. | |
| LPC (20:3) | lipid | 1 | — | — | Decreased LPC (20:3) content post-MI reflects phospholipid catabolism and myocardial dysfunction progression. | |
| LPE (18:2) | lipid | 1 | — | — | Decreased LPE (18:2) content post-MI reflects phospholipid catabolism and severity of myocardial ischemic injury. | |
| MARK4MARK4 | protein | 1 | — | ◆ | MARK4 is a microtubule-associated kinase released post-mortem and in severe cardiomyocyte injury during acute myocardial infarction. | |
| microRNA-133 | rna | 1 | — | — | miR-133 is released from ischemic cardiomyocytes during myocardial necrosis, serving as an early injury marker parallel to troponins. | |
| microRNA-134-5pMIR134 | rna | 1 | — | — | Circulating miR-134-5p released from ischemic myocardium serves as an early diagnostic biomarker for STEMI. | |
| microRNA-140-3p | rna | 1 | — | — | miR-140-3p is elevated in acute coronary syndrome and marks acute myocardial injury and ischemia. | |
| microRNA-181aMIR181A1 | rna | 1 | — | — | Circulating miR-181a reflects myocardial necrosis and inflammatory response in acute MI. | |
| microRNA-3149 | rna | 1 | — | — | miR-3149 is dysregulated during acute coronary syndrome and serves as a circulating injury biomarker. | |
| miR-106a | rna | 1 | — | — | miR-106a is elevated during acute myocardial injury. | |
| miR-106b-3p | rna | 1 | — | — | miR-106b-3p is elevated during acute myocardial injury and ischemic stress. | |
| miR-122-5p | rna | 1 | — | — | miR-122-5p circulates as a myocardial injury-release biomarker in acute MI, enabling early detection of cardiomyocyte necrosis. | |
| miR-133b | rna | 1 | — | — | A circulating microRNA downregulated in coronary artery disease that regulates myogenic differentiation and inflammatory responses in ischemic tissue. | |
| miR-142-5p | rna | 1 | — | — | miR-142-5p is elevated in acute myocardial injury and inflammatory stress. | |
| miR-144 | rna | 1 | — | — | Circulating miRNA biomarker associated with acute myocardial infarction onset and severity. | |
| miR-182-5p | rna | 1 | — | — | miR-182-5p differentially circulates in acute coronary syndromes, enabling classification of ACS subtypes and MI detection. | |
| miR-186 | rna | 1 | — | — | miR-186 dysregulation after MI associates with adverse myocardial remodeling and long-term mortality risk. | |
| miR-191 | rna | 1 | — | — | miR-191 is elevated in acute myocardial injury as a circulating biomarker. | |
| miR-203 | rna | 1 | — | — | miR-203 is an early circulating biomarker for STEMI onset, marking acute myocardial necrosis ahead of troponin rise. | |
| miR-208a | rna | 1 | — | — | miR-208a is released early from damaged myocardium during acute MI, providing an early detection window for cardiomyocyte injury. | |
| miR-210-3p | rna | 1 | — | — | miR-210-3p is upregulated in response to myocardial ischemia and hypoxia, differentiating MI from other acute cardiac presentations. | |
| miR-425-3p | rna | 1 | — | — | miR-425-3p is elevated in acute myocardial injury. | |
| miR-483-5p | rna | 1 | — | — | miR-483-5p is upregulated in acute myocardial injury and predicts adverse outcomes independent of troponin. | |
| miR-519e-5p | rna | 1 | — | — | miR-519e-5p expression pattern differentiates acute myocardial infarction from non-infarction ischemia, reflecting cardiomyocyte injury specificity. | |
| miR-629 | rna | 1 | — | — | miR-629 is elevated during acute myocardial injury. | |
| miR-889 | rna | 1 | — | — | miR-889 is elevated in acute myocardial injury. | |
| miR-96-5p | rna | 1 | — | — | miR-96-5p is elevated in acute myocardial infarction and regulates cardiomyocyte apoptosis through suppression of anti-apoptotic BCL2L13. | |
| miRNA-210 | rna | 1 | — | — | A hypoxia-inducible microRNA upregulated in response to myocardial ischemia that serves as an early diagnostic marker of acute coronary syndrome. | |
| Monocarboxylate transporter 1SLC16A1 | gene | 1 | — | ◆ | MCT1-mediated succinate and lactate efflux during reperfusion reflects cardiomyocyte metabolic dysregulation and injury. | |
| MR-PAMP | protein | 1 | — | — | MR-PAMP is a myocyte-derived danger signal released during cardiomyocyte necrosis in acute myocardial infarction. | |
| MYDGFMYDGF | protein | 1 | — | ◆ | MYDGF enhances myocyte survival and cardiac repair following Type 1 MI ischemia. | |
| Myosin Heavy Chain 7MYH7 | gene | 1 | — | ◆ | MYH7 upregulation reflects myocardial injury and dysfunction following ischemic necrosis in acute MI. | |
| MYOZ1MYOZ1 | gene | 1 | — | — | MYOZ1 influences cardiomyocyte structural adaptation and remodeling in response to ischemic injury and heart failure. | |
| N-Acetyl-L-leucine | metabolite | 1 | — | — | N-Acetyl-L-leucine differentiates atherothrombotic MI from supply-demand mismatch, reflecting myocardial amino acid remodeling. | |
| NADH Dehydrogenase Ubiquinone Iron-Sulfur Protein 8NDUFA8 | gene | 1 | — | ◆ | NDUFA8 mutations or dysregulation impair mitochondrial energy production, exacerbating cardiomyocyte ischemic injury during acute MI. | |
| NADPH oxidase 4NOX4 | gene | 1 | — | ◆ | NOX4-driven NADPH oxidase activity amplifies oxidative stress and myocardial injury during ischemia-reperfusion. | |
| NestinNES | protein | 1 | — | — | Nestin marks neovessel formation in the infarction zone, indicating cardiomyocyte injury and myocardial remodeling. | |
| NFU1 iron-sulfur cluster scaffoldNFS1 | gene | 1 | — | ◆ | NFS1 loss impairs iron-sulfur cluster biogenesis, promoting ferroptotic cardiomyocyte injury in acute MI. | |
| NMDAR | protein | 1 | — | — | NMDAR activation mediates excitotoxic calcium overload and mitochondrial damage in ischemic myocardial injury. | |
| Nonanoylcarnitine | metabolite | 1 | — | — | Nonanoylcarnitine elevation indicates myocardial fatty-acid oxidation perturbation and identifies acute myocardial infarction. | |
| NRASNRAS | gene | 1 | — | ◆ | NRAS modulates pathways governing cardiomyocyte ischemia and injury response during acute MI. | |
| NRK-2 | protein | 1 | — | — | NRK-2 mediates metabolic adaptation and survival signaling in ischemic myocardium, potentially modulating cardiomyocyte injury severity. | |
| Nuclear Receptor Coactivator 4NCOA4 | protein | 1 | — | ◆ | NCOA4 is the selective autophagy receptor for ferritin degradation, controlling labile iron pools and oxidative stress in ischemic cardiomyocytes. | |
| PC (18:2) | lipid | 1 | — | — | Decreased phosphatidylcholine (18:2) content post-MI reflects myocardial membrane degradation and cardiomyocyte injury. | |
| PC (20:0/20:3) | lipid | 1 | — | — | Decreased PC (20:0/20:3) content post-MI reflects myocardial membrane lipid catabolism and cardiomyocyte injury severity. | |
| PC (20:3/20:4) | lipid | 1 | — | — | Decreased PC (20:3/20:4) content post-MI reflects eicosanoid-precursor lipid depletion and myocardial dysfunction. | |
| PC(22:4/14:1) | lipid | 1 | — | — | Phosphatidylcholine dysregulated in myocardial ischemic injury and post-MI heart failure progression. | |
| PDE4D-interacting protein p6 | rna | 1 | — | — | A circulating RNA species that is differentially expressed in NSTEMI and serves as an early diagnostic marker of myocardial injury. | |
| PDK1PDK1 | protein | 1 | — | ◆ | PDK1 shifts myocardial metabolism toward glycolysis during ischemia, limiting oxidative stress and cardiomyocyte necrosis. | |
| PE (P-20:0/18:0) | lipid | 1 | — | — | Decreased plasmalogen PE (20:0/18:0) content post-MI reflects oxidative stress-induced myocardial membrane degradation. | |
| PE (P-20:1/18:0) | lipid | 1 | — | — | Decreased plasmalogen lipid content post-MI reflects oxidative damage to myocardial membranes and cardiomyocyte injury severity. | |
| PE(12:1e/22:0) | lipid | 1 | — | — | Phosphatidylethanolamine plasmalogen dysregulated in myocardial injury and post-MI heart failure. | |
| PELATON | rna | 1 | — | — | PELATON is a circulating RNA whose expression is dysregulated in acute coronary syndromes and may reflect either myocardial injury or vascular inflammation. | |
| Pentadecanoic acid (C15:0) | metabolite | 1 | — | — | Ischemia-reperfusion injury triggers fatty acid mobilization and mitochondrial lipid catabolism. | |
| Perforin 1PRF1 | gene | 1 | — | ◆ | PRF1 is a T cell cytotoxin that contributes to post-MI myocardial injury and dysfunction. | |
| PG (18:1/18:1) | lipid | 1 | — | — | Increased PG (18:1/18:1) content post-MI reflects cardiolipin metabolism alterations and myocardial ischemic injury. | |
| Phenylalanine | metabolite | 1 | — | — | Branched amino acid dysregulation in acute myocardial infarction marks ischemic metabolic failure and tissue injury. | |
| Phosphatidylethanolamine plasmalogen | lipid | 1 | — | — | Phosphatidylethanolamine plasmalogen provides antioxidant cardioprotection during myocardial ischemia-reperfusion injury. | |
| Phosphatidylinositol phosphate | lipid | 1 | — | — | Phosphatidylinositol phosphate dysmetabolism during MI reflects impaired phosphoinositide signaling and endothelial activation. | |
| Phosphatidylinositol Transfer Protein BetaPITPNB | gene | 1 | — | — | PITPNB phosphorylation reflects lipid-signaling dysfunction in ischemic cardiomyocyte injury. | |
| piRNA | rna | 1 | — | — | piRNAs are emerging circulating biomarkers in CVD; their role in MI appears linked to myocardial injury and inflammatory activation. | |
| PLIN1PLIN1 | gene | 1 | — | ◆ | PLIN1 (perilipin-1) regulates myocardial lipid homeostasis and provides cardioprotection by reducing ischemic injury. | |
| Protein Phosphatase ME1PPME1 | gene | 1 | — | ◆ | PPME1 differential regulation distinguishes ischemic Type 1 MI from pressure-overload cardiomyopathy. | |
| PYCR1PYCR1 | gene | 1 | — | ◆ | PYCR1 (pyrroline-5-carboxylate reductase 1) catalyzes proline synthesis and offers cardioprotection, reducing myocardial infarction severity. | |
| Regenerating Islet-Derived Protein 1 AlphaREG1A | protein | 1 | — | ◆ | REG1A is an acute-phase regenerative protein elevated in acute myocardial infarction, possibly supporting tissue recovery. | |
| RNA component of mitochondrial RNA processing | rna | 1 | — | — | RMRP is a circulating non-coding RNA that discriminates acute MI subtypes and detects acute myocardial injury in coronary syndromes. | |
| RNF207RNF207 | gene | 1 | — | — | RNF207 is a cardiac-specific ubiquitin ligase released upon cardiomyocyte injury and necrosis in acute myocardial infarction. | |
| S-Methylglutathione | metabolite | 1 | — | — | S-Methylglutathione reflects cardiomyocyte oxidative stress and ischemic injury during acute myocardial infarction. | |
| SEC31 Homolog ASEC31A | gene | 1 | — | ◆ | SEC31A differential expression distinguishes ischemic Type 1 MI pathophysiology from hemodynamic overload. | |
| Slit homolog 2SLIT2 | protein | 1 | — | ◆ | SLIT2 is a post-MI cardiac fibroblast-derived paracrine mediator involved in myocardial repair and remodeling. | |
| SM (d18:1/22:0) | lipid | 1 | — | — | Decreased sphingomyelin content post-MI reflects myocardial lipid catabolism and severity of cardiomyocyte injury and dysfunction. | |
| Small nucleolar RNA host gene 15 | rna | 1 | — | — | SNHG15 is a circulating long noncoding RNA that increases during acute coronary syndromes, serving as an ACS detection biomarker. | |
| Small nucleolar RNA host gene 5 | rna | 1 | — | — | SNHG5 is a circulating long noncoding RNA dysregulated in acute coronary syndromes, enabling early ACS detection. | |
| Solute carrier family 1 member 5SLC1A5 | gene | 1 | — | ◆ | SLC1A5 dysregulation in AMI impairs glutamate/cystine exchange, accelerating ferroptotic cardiomyocyte death. | |
| Stem cell antigen-1LY6A | protein | 1 | — | — | Sca-1+ progenitor cells are mobilized and recruited to infarcted myocardium to support tissue repair and regeneration. | |
| Tetraspanin-33TSPAN33 | protein | 1 | — | ◆ | TSPAN33 downregulation in acute MI reflects cardiomyocyte injury and loss of tetraspanin surface expression. | |
| Threonine | metabolite | 1 | — | — | Altered plasma amino acid metabolism reflects acute myocardial ischemic stress and cardiomyocyte injury. | |
| Threoninyl-glycine | metabolite | 1 | — | — | Threoninyl-glycine elevation identifies acute myocardial infarction and discriminates cardiac-risk phenotypes in acute coronary syndromes. | |
| TRIM54TRIM54 | gene | 1 | — | ◆ | TRIM54 is a cardiac-specific TRIM family E3 ligase upregulated during myocardial ischemia and necrosis in acute myocardial infarction. | |
| TRIM63TRIM63 | gene | 1 | — | — | TRIM63 (MURF1) is a cardiac-specific E3 ubiquitin ligase released during cardiomyocyte necrosis and protein degradation in acute myocardial infarction. | |
| Tripartite motif-containing protein 72TRIM72 | gene | 1 | — | ◆ | TRIM72 controls myocardial injury response and regenerative repair after ischemia. | |
| Tryptophol | metabolite | 1 | — | — | An alternative tryptophan catabolite serving as a myocardial-injury marker in STEMI. | |
| UCA1UCA1 | rna | 1 | — | — | Long non-coding RNA urothelial carcinoma-associated 1 dysregulated in acute myocardial infarction diagnosis. | |
| Urotensin-related peptide | peptide | 1 | — | — | A vasoactive peptide released during myocardial injury that serves as a biomarker in acute myocardial infarction. | |
| Valine | metabolite | 1 | — | — | Ischemic stress alters branched-chain amino acid metabolism and protein turnover in cardiomyocytes. | |
| Voltage-dependent anion channel 2VDAC2 | gene | 1 | — | ◆ | VDAC2 dysfunction promotes ferroptotic cell death in cardiomyocytes during ischemia-reperfusion injury after myocardial infarction. | |
| Xin Actin-Binding Repeat Protein 2XIRP2 | gene | 1 | — | ◆ | XIRP2 upregulation indicates cardiomyocyte structural remodeling and injury response in acute MI. | |
| XISTXIST | rna | 1 | — | — | XIST is a circulating long non-coding RNA elevated during acute myocardial injury and ischemia. | |
| YTH Domain Family Member 1YTHDF1 | protein | 1 | — | ◆ | YTHDF1 reads m6A methylation marks on ferritinophagy-related transcripts, modulating iron metabolism and oxidative stress in ischemic myocardium. | |
| YTH Domain Family Member 3YTHDF3 | protein | 1 | — | ◆ | YTHDF3 reads m6A methylation marks on ferritinophagy-related transcripts, modulating iron metabolism and oxidative stress in ischemic myocardium. | |
| Myosin Light Chain 2MYL2 | gene | — | — | ✦◆ | Cardiac MYL2 release reflects myocardial injury and cardiomyocyte necrosis/apoptosis post-MI. |
The whole atlas, at a glance
Step distribution, evidence coverage, molecule type & placement confidence — click into any slice.
Which markers actually separate the two
Type 1-vs-Type 2 discrimination scored on four axes — rupture (R), coronary (C), analytic (A) and evidence (E) — into a single T1 discrimination index.
| Marker | R | C | A | E | T1DI |
|---|---|---|---|---|---|
| CK-MBCKM | 66.70 | 50.00 | 96.00 | 100.00 | 67.50 |
| Cardiac troponin ITNNI3 | 100.00 | 58.30 | 96.00 | 78.00 | 62.00 |
| Creatine kinase-MB | 100.00 | 66.70 | 96.00 | 85.70 | 59.80 |
| Creatine Kinase | 66.70 | 71.40 | 96.00 | 100.00 | 57.30 |
| Troponin TTNNT2 | 100.00 | 60.00 | 96.00 | 85.00 | 57.10 |
| Cardiac troponins | 100.00 | 66.70 | 68.00 | 100.00 | 53.50 |
Ranked by diagnostic utility
Weight the axes to your question and the whole catalog re-ranks live — the markers most worth measuring float to the top.
Search all 1,969 molecules
Filter by cascade step, molecule type and evidence; click any molecule for its full evidence page.
How it was built
A reproducible, ground-up pipeline — from literature harvest to confident pathway placement.