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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 non-Type I discrimination

ScoresNon-Type-I-associated
R — rupture / Type-I
—
C — non-Type-I
67
A — assay feasibility
52
E — evidence strength
42
T1DI (composite)
5
Specificity differential (R−C)-51.7
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.
2sepsis / systemic inflammationmag 2
2anemia / acute blood lossn/a
2hypovolemia / dehydrationn/a
2tachyarrhythmiamag 2
2hypoxemia / respiratory failuremag 2
2hypertensive emergencyn/a
2high-demand / peri-operative stressmag 2
3sudden cardiac deathn/a
4aPCI-related periproceduraln/a
4bstent thrombosisn/a
4cin-stent restenosismag 2
5CABG-relatedmag 2
Coverage: 6/12 axes with evidence
Tier: deep-scored (abstract-extracted) · 17 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)