ADAMTS (含 Ⅰ 型血小板结合蛋白基序的解聚蛋白样金属蛋白酶)

ADAMTS is a class of zinc-dependent secreted metalloproteases that primarily participate in extracellular matrix (ECM) degradation and remodeling, blood coagulation regulation, and cardiovascular homeostasis. This family consists of 19 ADAMTS proteases and 7 ADAMTS-like proteins, each with distinct biological functions. Among them, ADAMTS1, 4, and 5 are responsible for proteoglycan degradation, ADAMTS2, 3, and 14 facilitate procollagen processing, ADAMTS13 regulates coagulation by cleaving von Willebrand factor (vWF), and ADAMTS7 and 12 influence vascular smooth muscle cell migration, contributing to atherosclerosis. Additionally, ADAMTS1 and ADAMTS8 function as tumor suppressors, inhibiting angiogenesis and thereby restricting tumor growth. Dysregulation of ADAMTS functions is associated with various diseases. For example, mutations in ADAMTS2 lead to Ehlers-Danlos syndrome (a connective tissue disorder with skin hyperelasticity) due to impaired collagen maturation; excessive ADAMTS5 activity disrupts proteoglycan homeostasis and exacerbates osteoarthritis; ADAMTS13 deficiency causes thrombotic thrombocytopenic purpura (TTP), resulting in abnormal blood clot formation. Additionally, ADAMTS7 promotes vascular remodeling, accelerating atherosclerosis progression. Therefore, selective inhibitors or activators targeting ADAMTS have emerged as potential therapeutic strategies for joint diseases, thrombotic disorders, and cardiovascular conditions^[1].