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Triglyceride-rich lipoprotein
Pathway / Lipid retention & oxidation

Triglyceride-rich lipoprotein

lipoprotein

Triglyceride-rich lipoprotein accumulation in subendothelium initiates lipid oxidation and atherogenic inflammation driving atherothrombotic MI.

Pathway placement
Cascade stepLipid retention & oxidation
Confidencehigh
RationaleCausal atherogenic remnant particles; promote atherosclerosis and vascular toxicity via subendothelial retention.
Also acts inVascular inflammation
Druggability
Not assessed (no mapped human gene target).

Type I vs non-Type I discrimination

ScoresLow-confidence (proxy)
R — rupture / Type-I
32
C — non-Type-I
43
A — assay feasibility
82
E — evidence strength
16
T1DI (composite)
6
Specificity differential (R−C)-11.3
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

Specialized reference method
Specimen
Serum or plasma (EDTA)
Collection tube
K2/K3-EDTA (lavender-top) · Serum separator (gold/red-top, SST)
Method / principle
NMR lipoprotein particle analysis or density-gradient ultracentrifugation
Reagent / substrate
No chemical reagent — NMR spectral deconvolution of lipid methyl signals (or ultracentrifugal separation by density)
Platform
NMR (LabCorp NMR LipoProfile) / analytical ultracentrifuge
Turnaround · availability
Send-out · Specialized reference lab

Literature evidence(3)