ADAMTS7 is a metalloproteinase with thrombospondin type 1 motif that plays a critical role in cardiovascular and joint disease pathogenesis 1. As a secreted extracellular matrix protease, ADAMTS7 degrades multiple ECM substrates to modulate disease progression 2. In atherosclerosis, ADAMTS7 expression is elevated in unstable plaques 3. The primary mechanism involves ADAMTS7-mediated degradation of tissue inhibitor of metalloprotease-1 (TIMP-1), which reduces TIMP-1's inhibitory effects on MMP-9 3. This promotes collagen degradation and plaque destabilization 3. ADAMTS7 also degrades COMP and thrombospondin-1, inhibiting vascular smooth muscle cell migration 4. Genome-wide association studies consistently link ADAMTS7 variants to coronary artery disease and aortic stenosis risk across multiple ethnic groups 15, with disease-associated variants acting through regulatory effects in smooth muscle cells 6. In osteoarthritis, enhanced chondrocyte fatty acid oxidation transcriptionally activates ADAMTS7, contributing to cartilage degradation and disease progression 7. Additionally, ADAMTS7 immunomodulatory functions may enhance anti-tumor immunity in select cancer contexts 8. Therapeutically, ADAMTS7 inhibition or vaccination against ADAMTS7 reduces atherosclerotic lesion formation and post-injury restenosis in preclinical models 43, making it an attractive therapeutic target.