ADAMTS1 is a multidomain extracellular metalloprotease that cleaves extracellular matrix proteoglycans, including aggrecan and versican, playing critical roles in both physiological and pathological processes 1. The enzyme possesses angiogenic inhibitor activity 1 and is involved in follicular rupture and ovulation, where decreased expression impairs cumulus expansion and oocyte maturation in polycystic ovary syndrome 2. In liver disease, hepatic endothelial cells produce ADAMTS1 in extracellular vesicles through epigenetic regulation, promoting fibrogenic immune cell recruitment and liver fibrosis progression in nonalcoholic steatohepatitis 3. ADAMTS1-mediated latent TGF-β1 activation via proteoglycan cleavage contributes to hepatic fibrosis, while extracellular matrix protein 1 antagonizes this pathway 4. In renal cell carcinoma, elevated ADAMTS1 drives anoikis resistance and invasion through versican V1 proteolysis, triggering EGFR transactivation and establishing a oncogenic feedback loop 5. Post-myocardial infarction, ADAMTS1 upregulation in endothelial cells exacerbates pathological scar formation via integrin α8-mediated mechanotransduction in cardiac fibroblasts 6. ADAMTS1 exhibits context-dependent roles: tumor-promoting in cancer through extracellular matrix remodeling, yet tissue-protective through angiogenic inhibition and matrix organization 7.