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Cholesteryl esters
Pathway / Lipid retention & oxidation

Cholesteryl esters

lipid

Cholesteryl esters accumulate in foam cells and atherogenic lipoproteins, driving plaque formation and remodeling post-MI.

Pathway placement
Cascade stepLipid retention & oxidation
Confidencehigh
RationaleCore lipidome of atherogenic lipoproteins and foam cells; plaque lipid composition; MI risk marker.
Also acts inVascular inflammation, Myocardial injury
Druggability
Not assessed (no mapped human gene target).

Type I vs non-Type I discrimination

ScoresLow-confidence (proxy)
R — rupture / Type-I
44
C — non-Type-I
54
A — assay feasibility
40
E — evidence strength
22
T1DI (composite)
4
Specificity differential (R−C)-9.5
Non-Type-I axis panel
Does this marker also move in each non-Type-I setting? mag 0–3; higher means less Type-I-specific. n/a = no evidence retrieved, which is not the same as no change.
No non-Type-I axis evidence retrieved.
Tier: light (literature co-occurrence proxy — lower confidence). See the discrimination table for all markers.

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)