All molecules
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1,969 molecules
| Molecule | Type | Pathway step | Conf. | Refs ▼ | Trials | Omics | Evidence | Mechanism |
|---|---|---|---|---|---|---|---|---|
LDL cholesterol | lipoprotein | Lipid entry/oxidation | high | 60 | 6 | — | — | LDL accumulation in the arterial intima is the initiating substrate of atherosclerotic plaque formation. |
Oxidized LDL | lipoprotein | Lipid entry/oxidation | high | 60 | 2 | — | — | Oxidized LDL drives plaque formation, inflammation, and endothelial dysfunction in atherothrombotic disease. |
HDL | lipoprotein | Lipid entry/oxidation | medium | 60 | — | — | — | HDL exerts atheroprotective effects via reverse cholesterol transport, antioxidant activity, and endothelial stabilization. |
C-reactive protein CRP | protein | Vascular inflammation | high | 60 | 8 | — | ✦◆ | hs-CRP is a systemic inflammatory marker reflecting plaque-driven inflammation and predicting atherothrombotic events. |
Interleukin-6 IL6 | protein | Vascular inflammation | high | 60 | 1 | — | ✦◆ | IL-6 promotes plaque inflammation and leukocyte recruitment, accelerating atherosclerotic instability and thrombotic risk. |
TNF-α TNF | protein | Vascular inflammation | high | 60 | 1 | — | ✦◆ | TNF-α is a pro-inflammatory cytokine that promotes atherosclerotic plaque inflammation, macrophage recruitment, endothelial dysfunction, and oxidative stress dr |
von Willebrand factor VWF | protein | Endothelial activation/erosion | high | 60 | — | — | ◆ | vWF exposure following endothelial activation enables platelet adhesion and thrombotic cascade initiation. |
P-selectin SELP | protein | Platelet activation | high | 60 | — | — | ✦◆ | P-selectin mediates platelet activation and adhesion to endothelium, driving thrombotic cascade in MI. |
D-dimer | protein | Coagulation / thrombus | high | 60 | 1 | — | — | D-dimer indicates active coagulation and thrombus formation during acute coronary events. |
Fibrinogen FGA | protein | Coagulation / thrombus | high | 60 | — | — | ◆ | Fibrinogen is the substrate for thrombin-driven fibrin polymerization forming the occlusive coronary thrombus. |
Plasminogen activator inhibitor-1 SERPINE1 | protein | Coagulation / thrombus | medium | 60 | — | — | ✦◆ | PAI-1 inhibits fibrinolysis and promotes a prothrombotic state favoring coronary thrombus formation and persistence. |
Cardiac troponin I TNNI3 | protein | Myocardial injury | high | 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, |
B-type natriuretic peptide NPPB | protein | Systemic / off-pathway | high | 60 | 1 | — | ✦◆ | BNP reflects post-infarction cardiac insufficiency and hemodynamic strain, operating off the atherothrombotic axis. |
Soluble CD40 ligand CD40LG | protein | Platelet activation | high | 59 | — | — | ✦◆ | sCD40L released from activated platelets amplifies endothelial dysfunction and platelet–leukocyte thrombotic crosstalk. |
Interleukin-1β IL1B | protein | Vascular inflammation | high | 57 | — | — | ◆ | Interleukin-1β is a central inflammasome-derived cytokine that orchestrates atherosclerotic plaque inflammation, promotes endothelial dysfunction and procoagula |
CK-MB CKM | protein | Myocardial injury | high | 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 |
Apolipoprotein B APOB | protein | Lipid entry/oxidation | high | 49 | 3 | — | ✦◆ | ApoB-containing lipoproteins are retained in the subendothelium and oxidatively modified, initiating atherogenesis. |
Thrombin-antithrombin complex | protein | Coagulation / thrombus | high | 48 | — | — | — | Thrombin-antithrombin complex is a marker of tissue-factor-triggered coagulation activation and thrombin generation, indicating active thrombus formation in acu |
Troponin T TNNT2 | protein | Myocardial injury | high | 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 |
Lipoprotein(a) LPA | lipoprotein | Lipid entry/oxidation | high | 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 |
sVCAM-1 VCAM1 | protein | Endothelial activation/erosion | high | 44 | — | — | ◆ | Soluble VCAM-1 is an endothelial adhesion molecule upregulated during endothelial activation and dysfunction; it mediates leukocyte recruitment into atheroscler |
Intercellular Adhesion Molecule 1 ICAM1 | protein | Endothelial activation/erosion | high | 43 | — | — | ◆ | sICAM-1 reflects endothelial activation and leukocyte recruitment to atherosclerotic plaques and coronary injury sites. |
Tissue Factor F3 | protein | Coagulation / thrombus | high | 41 | 1 | — | ◆ | Tissue Factor is exposed on thrombogenic lipid-core material after plaque rupture, triggering Factor VIIa and thrombin generation. |
Myeloperoxidase MPO | protein | Vascular inflammation | high | 40 | 1 | — | ✦◆ | Myeloperoxidase oxidizes LDL and generates reactive oxygen species in atherosclerotic plaques, promoting inflammation and endothelial dysfunction; also a marker |
Matrix metalloproteinase-9 MMP9 | protein | Cap degradation / rupture | high | 39 | — | — | ✦◆ | MMP-9 degrades extracellular matrix in the atherosclerotic fibrous cap, promoting rupture and thrombotic exposure. |
Growth differentiation factor 15 GDF15 | protein | Systemic / off-pathway | medium | 39 | — | — | ✦◆ | GDF15 reflects systemic stress, cardiac injury, and post-infarction remodeling, operating on a parallel outcome axis. |
Tissue plasminogen activator PLAT | protein | Coagulation / thrombus | high | 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 | Coagulation / thrombus | high | 37 | — | — | — | Fibrinopeptide A is released during thrombin-catalyzed fibrin polymerization, marking coagulation activation in coronary thrombosis. |
Platelet Factor 4 PF4 | protein | Platelet activation | high | 32 | — | — | ◆ | PF4 is released upon platelet activation and serves as an early biomarker of platelet recruitment and thrombus formation in Type 1 MI. |
Apolipoprotein A-I APOA1 | protein | Lipid entry/oxidation | high | 30 | 1 | — | ◆ | ApoA-I is the major HDL component mediating reverse cholesterol transport and endothelial protective effects; reduced levels indicate atherosclerotic burden. |
E-selectin SELE | protein | Endothelial activation/erosion | high | 30 | — | — | ◆ | E-selectin expression on endothelium marks activation and enables leukocyte rolling and adhesion during plaque inflammation and erosion. |
Prothrombin fragment 1+2 F2 | protein | Coagulation / thrombus | high | 29 | — | — | ✦◆ | F1+2 release quantifies activated prothrombin conversion, reflecting the rate of thrombin generation and coagulation activation. |
Interleukin-10 IL10 | protein | Vascular inflammation | medium | 28 | — | — | ◆ | Interleukin-10 is a protective anti-inflammatory cytokine that restrains atherosclerotic plaque inflammation and macrophage activation; its reduction by oxidize |
Apolipoprotein E APOE | protein | Lipid entry/oxidation | medium | 26 | — | 1 | ✦◆ | Apolipoprotein E is a lipoprotein structural protein and receptor ligand whose genetic polymorphisms influence LDL metabolism, lipoprotein retention, and athero |
PCSK9 PCSK9 | protein | Lipid entry/oxidation | high | 25 | 20 | 1 | ✦◆ | PCSK9 regulates LDL-receptor degradation, controlling LDL-C levels and subendothelial lipid retention underlying atherosclerosis. |
Beta-Thromboglobulin PPBP | protein | Platelet activation | high | 25 | — | 1 | ◆ | Beta-thromboglobulin is released upon platelet activation and serves as an early AMI biomarker of platelet recruitment. |
Integrin alpha IIb ITGA2B | protein | Platelet activation | high | 25 | — | — | ✦◆ | ITGA2B-encoded integrin αIIb subunit forms the αIIbβ3 receptor essential for platelet aggregation and coronary thrombus formation in Type 1 MI. |
Thrombin | protein | Coagulation / thrombus | high | 25 | 1 | — | — | Thrombin is generated by tissue-factor-triggered coagulation and drives fibrin polymerization and platelet activation in coronary thrombosis. |
Fibrinogen Beta Chain FGB | protein | Coagulation / thrombus | high | 25 | — | — | ◆ | Fibrinogen polymerizes into fibrin scaffolding the occlusive coronary thrombus and amplifies platelet aggregation. |
Lipoprotein-associated Phospholipase A2 PLA2G7 | protein | Vascular inflammation | high | 24 | 4 | — | ✦◆ | Lp-PLA2 generates inflammatory mediators from oxidized lipids within atherosclerotic plaques, promoting destabilization and rupture. |
Monocyte Chemoattractant Protein-1 CCL2 | protein | Vascular inflammation | high | 24 | — | — | ◆ | MCP-1 recruits monocytes to the atherosclerotic plaque and inflamed endothelium, sustaining plaque destabilization. |
Prothrombin Fragment 1+2 | protein | Coagulation / thrombus | high | 24 | — | — | — | Prothrombin fragment 1+2 is released during tissue-factor-triggered coagulation, indicating thrombin generation during coronary thrombosis. |
Lysophosphatidylcholine | lipid | Lipid entry/oxidation | medium | 23 | — | — | — | Lysophosphatidylcholine, a bioactive lipid species derived from lipoprotein remodeling, promotes atherosclerosis and altered lipid homeostasis in Type 1 MI. |
thrombomodulin THBD | protein | Endothelial activation/erosion | high | 23 | — | — | ◆ | Thrombomodulin shedding from damaged endothelium impairs anticoagulation and indicates endothelial erosion/dysfunction in acute coronary events. |
Lectin-like Oxidized LDL Receptor 1 | protein | Lipid entry/oxidation | high | 22 | — | — | — | LOX-1 mediates uptake of oxidized LDL by endothelial cells and macrophages, fueling plaque lipid accumulation and inflammation. |
Nitric oxide | metabolite | Endothelial activation/erosion | high | 22 | 3 | — | — | Nitric oxide produced by endothelial cells regulates vasodilation and suppresses platelet adhesion; reduced bioavailability reflects endothelial dysfunction and |
Endothelial nitric oxide synthase NOS3 | protein | Endothelial activation/erosion | high | 22 | — | — | ✦◆ | Endothelial NOS catalyzes NO production essential for vasodilation and platelet inhibition; dysfunction contributes to endothelial erosion and thrombosis. |
Very-Low-Density Lipoprotein | lipoprotein | Lipid entry/oxidation | high | 21 | — | — | — | VLDL, an apoB-containing atherogenic lipoprotein, accumulates in the arterial intima where it undergoes oxidative modification, initiating atherosclerotic plaqu |
Interleukin-18 IL18 | protein | Vascular inflammation | high | 21 | — | — | ◆ | Interleukin-18 is an inflammasome-processed cytokine that promotes atherosclerotic inflammation, immune activation, and plaque destabilization in the atherothro |
ST2 IL1RL1 | protein | Systemic / off-pathway | high | 21 | — | — | ◆ | ST2 signals myocardial stress and remodeling response post-infarction, serving as an off-pathway hemodynamic/mechanical stress indicator. |
Interleukin-8 CXCL8 | protein | Vascular inflammation | high | 20 | — | — | ✦◆ | IL-8 is released during plaque inflammation and endothelial activation, recruiting neutrophils and amplifying platelet activation. |
Vascular endothelial growth factor VEGFA | protein | Endothelial activation/erosion | medium | 20 | 1 | — | ◆ | VEGF promotes endothelial repair, angiogenesis and endothelial progenitor cell mobilization following myocardial injury and revascularization therapy. |
Glycoprotein VI GP6 | protein | Platelet activation | high | 20 | — | — | ✦◆ | GPVI binds exposed collagen upon cap rupture or erosion, triggering platelet adhesion, activation, and thrombus propagation. |
CD31 | protein | Endothelial activation/erosion | medium | 19 | — | — | — | CD31 marks endothelial cell activation and erosion in sEVs, indicating endothelial dysfunction and superficial erosion in Type 1 MI pathology. |
Fibrin | protein | Coagulation / thrombus | high | 19 | — | 1 | — | Fibrin polymerization forms the structural matrix of the occlusive coronary thrombus, with impaired fibrinolysis predicting worse outcomes. |
Phosphatidylcholine | lipid | Lipid entry/oxidation | high | 18 | — | — | — | Phosphatidylcholine species composition of lipoproteins and plaques reflects atherogenesis severity and plaque lipid core character. |
Adiponectin ADIPOQ | protein | Vascular inflammation | high | 18 | — | — | ◆ | Adiponectin suppresses plaque inflammation and endothelial dysfunction, exerting cardioprotection against atherothrombotic injury. |
Glycoprotein Ib GP1BA | protein | Platelet activation | high | 18 | — | — | ◆ | GPIb mediates platelet tethering to exposed von Willebrand factor at the site of endothelial rupture or erosion, initiating platelet adhesion and activation. |
H-FABP FABP3 | protein | Myocardial injury | high | 18 | 1 | — | ◆ | H-FABP is released early from myocardial ischemia and necrosis, serving as an early biomarker of cardiomyocyte injury in acute MI. |
Sphingomyelin | lipid | Lipid entry/oxidation | medium | 17 | — | — | — | Sphingomyelin alters LDL aggregation susceptibility and membrane integrity, contributing to lipid retention and oxidative modification in the atherosclerotic le |
LDL Receptor LDLR | gene | Lipid entry/oxidation | high | 17 | 3 | 1 | ✦◆ | LDLR mediates LDL endocytosis; mutations impair LDL clearance, driving lipid retention and accelerated atherogenesis. |
homocysteine | metabolite | Endothelial activation/erosion | medium | 17 | — | — | — | Elevated homocysteine impairs endothelial function and promotes oxidative modification of LDL, accelerating atherosclerotic lipid retention and plaque vulnerabi |
antithrombin III SERPINC1 | protein | Coagulation / thrombus | medium | 17 | — | — | ✦◆ | Antithrombin III is consumed during thrombin-driven thrombus formation, and its depletion indicates active coagulation in acute infarction. |
Cystatin C CST3 | protein | Systemic / off-pathway | high | 17 | — | — | ✦◆ | Cystatin C reflects glomerular filtration and renal function; elevated levels indicate cardiorenal risk and mortality in acute coronary syndrome. |
Ceramide | lipid | Lipid entry/oxidation | high | 16 | — | — | — | Ceramide is a pro-atherogenic bioactive lipid that drives altered lipid metabolism, LDL aggregation, foam-cell formation and atherosclerotic plaque progression. |
HDL cholesterol | lipoprotein | Lipid entry/oxidation | high | 16 | 1 | — | — | HDL removes cholesterol and phospholipid hydroperoxides from lesions, opposing atherosclerotic lipid accumulation. |
Plasminogen PLG | protein | Coagulation / thrombus | high | 16 | 1 | — | ✦◆ | Plasminogen activation to plasmin drives fibrin degradation and thrombus resolution in coronary occlusion. |
Triglycerides | lipid | Lipid entry/oxidation | high | 15 | 2 | — | — | Elevated triglycerides promote atherosclerotic lipid deposition and dysfunctional lipoprotein remodeling. |
NLRP3 inflammasome NLRP3 | protein | Vascular inflammation | medium | 15 | 1 | — | — | NLRP3 inflammasome activation in atherosclerotic plaques and post-MI inflammation generates IL-1β and IL-18, amplifying plaque destabilization and injury respon |
Thromboxane B2 | metabolite | Thromboxane / COX-1 | high | 15 | — | — | — | Thromboxane B2 is the stable inactive metabolite of thromboxane A2, a COX-1-generated eicosanoid that amplifies platelet recruitment and aggregation. |
Interferon-Gamma IFNG | protein | Vascular inflammation | high | 14 | — | — | ◆ | IFN-γ amplifies macrophage activation and vascular inflammation in destabilized atherosclerotic plaques preceding Type 1 MI. |
PECAM-1 PECAM1 | protein | Endothelial activation/erosion | medium | 14 | — | — | ✦◆ | PECAM-1 mediates endothelial cell–cell and endothelial–platelet adhesion; dysfunction reflects endothelial activation and increased thrombotic risk. |
Phosphatidylserine | lipid | Platelet activation | medium | 14 | — | — | — | Phosphatidylserine exposure on activated platelets and microparticles promotes platelet aggregation and thrombin generation. |
Factor VII F7 | protein | Coagulation / thrombus | high | 14 | — | — | ◆ | FVII activity initiates tissue-factor-mediated coagulation and fibrin-thrombus formation in MI. |
Copeptin AVP | peptide | Myocardial injury | high | 14 | 5 | — | ✦◆ | Copeptin is released in response to myocardial ischemia and necrosis, providing early detection of acute coronary syndrome alongside cardiomyocyte injury. |
Myoglobin MB | protein | Myocardial injury | high | 14 | — | — | ✦◆ | Myoglobin released from ischemic cardiomyocytes serves as an early biomarker of myocardial infarction and necrotic injury. |
Trimethylamine N-oxide | metabolite | Lipid entry/oxidation | high | 13 | — | — | — | TMAO promotes lipid oxidation, plaque inflammation and destabilization, increasing atherothrombotic rupture and thrombotic risk. |
Matrix Metalloproteinase-2 MMP2 | protein | Cap degradation / rupture | high | 13 | — | — | ◆ | MMP-2 degrades the fibrous cap and myocardial ECM, mediating plaque rupture and post-infarction ventricular remodeling. |
CD36 molecule CD36 | protein | Platelet activation | high | 13 | — | 1 | ◆ | CD36 acts as a platelet scavenger receptor for oxidized LDL, amplifying platelet activation and microvesicle formation during acute thrombosis. |
CD39 ENTPD1 | protein | Platelet activation | high | 13 | — | — | ◆ | CD39 ectonucleotidase hydrolyzes ATP and ADP to adenosine monophosphate, attenuating platelet activation and arterial thrombosis. |
arachidonic acid | metabolite | Thromboxane / COX-1 | high | 13 | — | — | — | Arachidonic acid elevation drives thromboxane-A2 generation and eicosanoid-mediated platelet aggregation and inflammation in acute MI. |
CD34 | protein | Endothelial activation/erosion | medium | 12 | — | 1 | — | Circulating CD34+ endothelial progenitor and endothelial cells mark endothelial erosion and reparative responses in MI. |
Fibronectin FN1 | protein | Platelet activation | high | 12 | — | — | ✦◆ | Fibronectin mediates platelet adhesion to exposed matrix and fibroblast paracrine signaling; dysregulation marks plaque instability and thrombotic coronary even |
Factor XI F11 | protein | Coagulation / thrombus | high | 12 | — | — | ◆ | Factor XI activation by thrombin and contact factors amplifies intrinsic coagulation in post-rupture and post-erosion thrombosis, driving coronary occlusion. |
Transforming Growth Factor-Beta TGFB1 | protein | Myocardial injury | medium | 12 | — | — | ✦◆ | TGF-β drives myocardial fibrosis and remodeling following ischemic injury and modulates plaque inflammation via foam cell formation. |
Serum Amyloid A SAA1 | protein | Vascular inflammation | high | 11 | — | — | ◆ | SAA is a major acute-phase protein elevated at plaque rupture, modifies HDL-mediated reverse cholesterol transport and amplifies vascular inflammation. |
Pregnancy-associated Plasma Protein A PAPPA | protein | Cap degradation / rupture | high | 11 | — | — | ✦◆ | PAPP-A is a metalloproteinase elevated in atherosclerotic plaques that degrades extracellular matrix, promoting cap rupture and thrombosis. |
Soluble lectin-like oxidized LDL receptor 1 OLR1 | protein | Endothelial activation/erosion | high | 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 Cadherin CDH5 | protein | Endothelial activation/erosion | high | 11 | — | — | ◆ | Vascular endothelial cadherin cleavage destabilizes endothelial junctions, enabling transmigration and exposing subendothelial matrix. |
phosphatidylethanolamine | lipid | Platelet activation | high | 11 | — | — | — | Phosphatidylethanolamine dysregulation in platelets and monocytes contributes to platelet dysfunction and pro-thrombotic extracellular vesicle release in Type 1 |
Adenosine diphosphate | metabolite | Platelet activation | high | 11 | 1 | — | — | ADP released from platelet dense granules activates P2Y receptors, sustaining platelet aggregation and thrombus propagation. |
Integrin αIIbβ3 | protein | Platelet activation | high | 11 | — | — | — | Integrin αIIbβ3 bridges platelets via fibrinogen binding, essential for platelet-dependent thrombus formation. |
Tissue factor pathway inhibitor TFPI | protein | Coagulation / thrombus | high | 11 | — | — | ◆ | Tissue factor pathway inhibitor antagonizes coagulation activation and thrombus formation, with inverse association to MI risk. |
Coagulation factor VIII F8 | protein | Coagulation / thrombus | medium | 11 | — | — | ◆ | Factor VIII elevation reflects a pro-coagulative state and augments the intrinsic tenase complex, increasing thrombin generation risk. |
Factor V F5 | protein | Coagulation / thrombus | high | 11 | — | — | ◆ | Factor V acts as a cofactor in the prothrombinase complex to amplify thrombin generation and drive fibrin polymerization during coronary thrombus formation. |
Ceramides | lipid | Lipid entry/oxidation | high | 10 | — | — | — | Ceramide elevation is a biomarker of atherosclerotic disease progression and cardiometabolic lipid stress in acute MI. |
Pentraxin-3 PTX3 | protein | Vascular inflammation | high | 10 | — | — | ✦◆ | Pentraxin-3 mediates immune inflammation in atherosclerotic plaques and modulates platelet activation during thrombosis. |
CD40 CD40 | gene | Vascular inflammation | high | 10 | — | — | ◆ | CD40–CD40L interaction promotes endothelial activation, leukocyte recruitment, and platelet–leukocyte thromboinflammatory crosstalk. |
S100A9 S100A9 | protein | Vascular inflammation | high | 10 | — | — | ◆ | S100A9 (calprotectin) is a key alarmin amplifying vascular inflammation and thromboinflammation through monocyte recruitment and neutrophil-platelet interaction |
S100A8 S100A8 | protein | Vascular inflammation | high | 10 | — | — | ◆ | S100A8 (calprotectin) drives sterile inflammation and thromboinflammation in acute MI, promoting infarct wall thinning and adverse remodeling. |
Interleukin-2 IL2 | protein | Vascular inflammation | medium | 10 | — | — | ◆ | IL-2 elevation promotes T-cell-mediated vascular inflammation and is associated with acute coronary syndrome. |
Interleukin-17A IL17A | protein | Vascular inflammation | high | 10 | — | — | ✦◆ | IL-17A is a pro-inflammatory T-cell cytokine that destabilizes plaques, activates platelets, and promotes coronary thrombosis in Type 1 MI. |
Collagen Type I Alpha 1 COL1A1 | protein | Cap degradation / rupture | medium | 10 | — | — | ◆ | COL1A1 is the major fibrous-cap structural protein; its exposure upon rupture initiates platelet adhesion and thrombosis. |
Coagulation Factor XII F12 | protein | Coagulation / thrombus | medium | 10 | — | — | ◆ | Factor XII activation in the contact system amplifies coagulation and contributes to thrombus formation and fibrinolytic-induced reactivation in MI. |
Protein C PROC | protein | Coagulation / thrombus | medium | 10 | — | — | ✦◆ | Protein C deficiency or inactivation impairs anticoagulant regulation, promoting prothrombotic thrombus formation in acute MI. |
tryptophan | metabolite | Systemic / off-pathway | medium | 10 | — | — | — | Tryptophan metabolism dysregulation associates with immune dysbalance and heightened atherosclerotic inflammation in MI risk, operating through systemic pathway |
Paraoxonase 1 PON1 | protein | Lipid entry/oxidation | high | 9 | — | — | ✦◆ | PON1 is an HDL-associated esterase that hydrolyzes oxidized phospholipids in LDL, preventing lipid-core accumulation and plaque inflammation. |
Apolipoprotein C3 APOC3 | protein | Lipid entry/oxidation | high | 9 | — | — | ◆ | ApoC3 on atherogenic remnants attenuates clearance and intensifies subendothelial lipid retention, plaque inflammation, and rupture risk in Type 1 MI. |
C-X-C Motif Chemokine Ligand 12 CXCL12 | protein | Vascular inflammation | high | 9 | — | — | ◆ | CXCL12 activates endothelial NF-κB signaling, recruits immune cells to atherosclerotic plaques, and mediates platelet–thrombosis interactions. |
CD14 CD14 | protein | Vascular inflammation | high | 9 | — | 1 | ✦◆ | CD14 marks monocyte and macrophage subsets that drive vascular inflammation, plaque destabilization, and contribute to platelet–leukocyte crosstalk during acute |
Toll-Like Receptor 4 TLR4 | protein | Vascular inflammation | high | 9 | — | 1 | ◆ | TLR4 promotes inflammasome signaling and oxidative stress in atherothrombotic plaque and platelets, driving MI progression. |
Thrombospondin-1 THBS1 | protein | Endothelial activation/erosion | medium | 9 | — | — | ◆ | Thrombospondin-1 mediates endothelial erosion and platelet-leukocyte engagement, modulating thrombus formation and post-MI inflammation. |
VEGFR-2 (KDR) KDR | protein | Endothelial activation/erosion | medium | 9 | — | — | ◆ | VEGFR-2 on circulating endothelial cells and EPCs marks endothelial activation, injury and angiogenic response in Type 1 MI. |
lactate dehydrogenase | protein | Myocardial injury | high | 9 | — | — | — | LDH is released from ischemic and necrotic myocardium during acute infarction, indicating cardiomyocyte death. |
Lipoprotein lipase LPL | protein | Lipid entry/oxidation | high | 8 | — | — | ✦◆ | Rate-limiting enzyme hydrolyzing triglycerides in atherogenic lipoproteins, regulated by ANGPTL inhibitors. |
Oxidized Phospholipids | lipid | Lipid entry/oxidation | high | 8 | — | — | — | Oxidized phospholipids generated from atherosclerotic lipid oxidation drive plaque inflammation and vascular cell activation in atherothrombotic cascade. |
CDKN2B CDKN2B | gene | Vascular inflammation | medium | 8 | — | — | ✦ | CDKN2B variants affect vascular cell proliferation and inflammatory signaling, modulating atherosclerotic plaque development and rupture risk. |
Osteopontin SPP1 | protein | Vascular inflammation | medium | 8 | — | — | ✦◆ | Osteopontin promotes macrophage-fibroblast crosstalk and collagen remodeling, destabilizing the plaque and driving post-MI cardiac remodeling. |
Uric acid | metabolite | Vascular inflammation | medium | 8 | — | — | — | Uric acid accumulates during oxidative injury and endothelial dysfunction in acute MI, serving as a biomarker of inflammatory burden and CAD severity. |
Endothelin-1 EDN1 | peptide | Endothelial activation/erosion | high | 8 | 1 | — | ◆ | ET-1 drives endothelial activation, excessive vasoconstriction, and endocardial injury during acute MI, with predictive value for endothelial progenitor cell mo |