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Transforming Growth Factor-Beta
Pathway / Myocardial injury (shared endpoint)

Transforming Growth Factor-Beta

TGFB1protein

TGF-β drives myocardial fibrosis and remodeling following ischemic injury and modulates plaque inflammation via foam cell formation.

Pathway placement
Cascade stepMyocardial injury (shared endpoint)
Confidencemedium
RationaleFibrosis and cardiac remodeling mediator post-MI; modulates foam cell formation.
Also acts inVascular inflammation, Endothelial activation/erosion, Platelet activation, Systemic / off-pathway, Cap degradation / rupture
Druggability
DruggableYes
Known drugs / candidates5
Small-molecule tractableYes
Antibody tractableYes
EnsemblENSG00000105329

Type I vs Type II discrimination

ScoresIndeterminate
R — rupture / Type-I
67
C — confounder / Type-II
42
A — assay feasibility
72
E — evidence strength
75
T1DI (composite)
34
Specificity differential (R−C)+25
Confounder panel (Type-II drivers)
1sepsis / systemic inflammationmag 2
2anemia / acute blood lossn/a
3hypovolemia / dehydrationmag 0
4tachyarrhythmiamag 2
5hypoxemia / respiratory failuren/a
6hypertensive emergencyn/a
7high-demand / peri-operative stressmag 1
Coverage: 4/7 confounders with evidence
Tier: deep-scored (abstract-extracted) · 16 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
Serum or plasma
Collection tube
Serum separator (gold/red-top, SST) · K2/K3-EDTA (lavender-top)
Method / principle
Sandwich immunoassay (ELISA) — research-grade unless a cleared assay exists
Reagent / substrate
Matched anti-target antibody pair (capture + labeled detection)
Platform
ELISA microplate or multiplex (Luminex/MSD)
Turnaround · availability
Send-out / research · Research-grade (no universal clinical assay)

Human genetic evidence

2
GWAS associations
Traits: myocardial infarction

Literature evidence(12)