Sclerostin
SOSTproteinSclerostin, a Wnt antagonist from bone, reflects post-MI cardiac remodeling and systemic stress responses independent of atherothrombotic progression.
Pathway placement
Cascade stepOff-pathway / systemic markers
Confidencemedium
RationaleBone-derived remodeling marker; systemic axis distinct from atherothrombotic cascade.
Druggability
Not assessed (no mapped human gene target).
Type I vs Type II discrimination
ScoresLow-confidence (proxy)
R — rupture / Type-I37
C — confounder / Type-II58
A — assay feasibility68
E — evidence strength22
T1DI (composite)6
Specificity differential (R−C)-20.9
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
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)
Literature evidence(2)
- Observational and Mendelian randomization studies of plasma sclerostin levels do not provide evidence of cardiovascular adverse effects of sclerostin inhibition.Human molecular genetics · 2026 · PMID 41324467 · doi
- In-depth proteomics approach reveals novel biomarkers of cardiac remodelling after myocardial infarction: An exploratory analysis.Journal of cellular and molecular medicine · 2020 · PMID 32701210 · doi