ADAMTS4
ADAMTS4proteinADAMTS4 metalloprotease degrades versican and other proteoglycans in the atherosclerotic plaque extracellular matrix, promoting fibrous-cap thinning and remodeling.
Pathway placement
Cascade stepFibrous-cap degradation & rupture
Confidencemedium
RationaleADAMTS metalloprotease degrades extracellular matrix; vascular remodeling and fibrous-cap destabilization.
Also acts inVascular inflammation
Druggability
DruggableYes
Known drugs / candidates0
Small-molecule tractableYes
Antibody tractableYes
EnsemblENSG00000158859
Type I vs Type II discrimination
ScoresLow-confidence (proxy)
R — rupture / Type-I23
C — confounder / Type-II47
A — assay feasibility68
E — evidence strength18
T1DI (composite)5
Specificity differential (R−C)-23.3
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)
- Oxidized LDL-mediated upregulation of ADAMTS-4 in monocytes/macrophages involves ROS-NF-κB-SIRT-1 pathway.Physiology international · 2023 · PMID 37216221 · doi
- ADAMTS4 level in patients with stable coronary artery disease and acute coronary syndromes.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2009 · PMID 19944557 · doi