lysophosphatidylethanolamine
lipidLysophosphatidylethanolamine dysregulation in monocytes and plaques associates with CAD risk, plaque burden, and acute coronary events.
Pathway placement
Cascade stepLipid retention & oxidation
Confidencehigh
RationaleAltered in CAD and AMI; plaque composition modulation; unsaturated species CAD risk.
Also acts inVascular inflammation, Coagulation / thrombus
Druggability
Not assessed (no mapped human gene target).
Assay & specimen
Class-level default (no specific cleared assay)— generic method inferred from analyte class; confirm against a specific product insert before use.
Specimen
Serum or plasma (EDTA to limit oxidation)
Collection tube
K2/K3-EDTA (lavender-top) · Serum separator (gold/red-top, SST)
Method / principle
LC-MS/MS lipidomics (targeted or shotgun)
Reagent / substrate
Deuterated lipid-class internal standards; MS/MS transitions
Platform
LC-MS/MS
Turnaround · availability
Research · Research-only
Literature evidence(5)
- Changes to the serum lipidome and their relation to coronary plaque in the first six months after acute myocardial infarction.Atherosclerosis · 2025 · PMID 40651072 · doi
- Lipidomics analysis of monocytes from patients with acute myocardial infarction reveals lactosylceramide as a new player in monocyte migration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021 · PMID 33856696 · doi
- Lysophospholipids as Predictive Markers of ST-Elevation Myocardial Infarction (STEMI) and Non-ST-Elevation Myocardial Infarction (NSTEMI).Metabolites · 2020 · PMID 33396480 · doi
- Lipidomic analysis of plasma lipoprotein fractions in myocardial infarction-prone rabbits.Journal of bioscience and bioengineering · 2015 · PMID 26162515 · doi
- Alteration in metabolic signature and lipid metabolism in patients with angina pectoris and myocardial infarction.PloS one · 2015 · PMID 26258408 · doi