miR-143-3p
rnamiR-143-3p targets vascular proteins involved in smooth-muscle contractility and platelet adhesion, modulating the thrombotic response to plaque rupture.
Pathway placement
Cascade stepPlatelet adhesion & activation
Confidencemedium
RationaleRegulates vascular smooth muscle phenotype and platelet function.
Also acts inVascular inflammation
Druggability
Not assessed (no mapped human gene target).
Type I vs Type II discrimination
ScoresLow-confidence (proxy)
R — rupture / Type-I20
C — confounder / Type-II43
A — assay feasibility50
E — evidence strength16
T1DI (composite)3
Specificity differential (R−C)-22.5
Confounder panel (Type-II drivers)
No confounder 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
Whole blood or cell-free plasma
Collection tube
PAXgene/Tempus RNA tube · K2/K3-EDTA (lavender-top)
Method / principle
RT-qPCR (TaqMan) or small-RNA sequencing
Reagent / substrate
Target-specific primers/probe; reverse transcriptase (miRNA: stem-loop RT primer)
Platform
qPCR instrument / NGS
Turnaround · availability
Research / send-out · Research (few LDTs)
Literature evidence(1)
- Genome-wide identification of circulating-miRNA expression quantitative trait loci reveals the role of several miRNAs in the regulation of cardiometabolic phenotypes.Cardiovascular research · 2019 · PMID 30715214 · doi