Atherosclerotic cardiovascular disease (ASCVD) is an inflammatory disease characterized by extensive arterial wall matrix protein degradation. Cysteine protease cathepsins play a pivotal role in extracellular matrix (ECM) remodeling and have been implicated in the development and progression of atherosclerosis-based cardiovascular diseases. An imbalance in expression between cathepsins (such as cathepsins S, K, L, C) and their inhibitor cystatin C may favor proteolysis of ECM in the pathogenesis of cardiovascular disease such as atherosclerosis, aneurysm formation, restenosis, and neovascularization. New insights into cathepsin functions have been made possible by the generation of knockout mice and by the application of specific inhibitors. Inflammatory cytokines regulate the expression and activities of cathepsins in cultured vascular cells and macrophages. In addition, evaluations of the possibility of cathepsins as a diagnostic tool revealed that the circulating levels of cathepsin S, K, and L, and their endogenous inhibitor cystatin C could be promising biomarkers in the diagnosis of coronary artery disease, aneurysm, adiposity, peripheral arterial disease, and coronary artery calcification. In this review, we summarize the available information regarding the mechanistic contributions of cathepsins to ASCVD.
[1]Fudan Univ, Zhongshan Hosp, Shanghai Inst Cardiovasc Dis, Shanghai, Peoples R China.
[2]Tongji Univ, Tongji Hosp, Dept Nephrol, Shanghai, Peoples R China.
[3]Shanghai Jiao Tong Univ, Shanghai Gen Hosp, Sch Med, Dept Cardiol, Shanghai, Peoples R China.
[4]Yanbian Univ Hosp, Dept Cardiol, 1327 Juzijie, Yanji 133000, Peoples R China.
[5]Nagoya Univ, Grad Sch Med, Inst Innovat Future Soc, Nagoya, Aichi, Japan.
[6]Kyung Hee Univ, Kyung Hee Univ Hosp, Dept Internal Med, Div Cardiol, Seoul, South Korea.
(8.0+极速模式)