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SMAD3
Pathway / Plaque inflammation

SMAD3

SMAD3gene

SMAD3 is a CAD-risk effector in smooth muscle cells that controls TGF-β-mediated inflammation, matrix remodeling, and fibrous-cap stability.

Pathway placement
Cascade stepPlaque inflammation
Confidencemedium
RationaleTGF-β signaling in SMCs; regulates inflammation, fibrosis, and cap stability.
Also acts inCap degradation / rupture, Endothelial activation/erosion
Druggability
DruggableYes
Known drugs / candidates0
Small-molecule tractableYes
Antibody tractableYes
EnsemblENSG00000166949

Type I vs Type II discrimination

ScoresType-II-associated
R — rupture / Type-I
—
C — confounder / Type-II
67
A — assay feasibility
52
E — evidence strength
42
T1DI (composite)
5
Specificity differential (R−C)-51.7
Confounder panel (Type-II drivers)
1sepsis / systemic inflammationmag 2
2anemia / acute blood lossn/a
3hypovolemia / dehydrationn/a
4tachyarrhythmiamag 2
5hypoxemia / respiratory failuremag 2
6hypertensive emergencyn/a
7high-demand / peri-operative stressmag 2
Coverage: 4/7 confounders with evidence
Tier: deep-scored (abstract-extracted) · 18 supporting references. 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 — gene is not a circulating analyte; measure protein product or genotype
Collection tube
K2-EDTA whole blood (lavender-top)
Method / principle
SNP genotyping / sequencing; or immunoassay of encoded protein
Reagent / substrate
Allele-specific primers/probes (TaqMan) or NGS panel; or antibody for protein
Platform
qPCR / NGS / array
Turnaround · availability
Send-out · Genotyping widely available; protein assay variable

Human genetic evidence

3
GWAS associations
Traits: myocardial infarction

Literature evidence(3)