SIRT3
锡尔图因
线粒体
乙酰化
生物
细胞生物学
西妥因1
作者
Mengfei Cao,Qianru Zhao,Xia Sun,Han Qian,Shumei Lyu,Rui Chen,Hao Xia,Wei Yuan
标识
DOI:10.1016/j.freeradbiomed.2022.01.005
摘要
Acetylation is one of the most important methods of modification that lead to a change in the function of proteins. In humans, metabolic enzymes commonly undergo acetylation, which regulates the activities of metabolic enzymes and metabolic pathways. Sirtuin 3 (SIRT3) is a prominent deacetylase that participates in mitochondrial metabolism, redox balance, and mitochondrial dynamics by regulating mitochondrial protein acetylation, thereby protecting mitochondria from damage. Normal mitochondrial function is essential for maintaining the metabolism and function of the heart. Therefore, mitochondrial dysfunction caused by SIRT3 consumption and defects leads to the development of a variety of cardiovascular diseases. A comprehensive understanding of the role of SIRT3 in cardiovascular disease is critical for developing new therapeutic strategies. Herein, we summarize the function of SIRT3 in mitochondria, the complex mechanisms mediating cardiovascular diseases, and the potential value of SIRT3 small-molecule agonists in future clinical treatments. • Sirtuin 3 participates in mitochondrial metabolism, redox balance, and mitochondrial dynamics by regulating deacetylation. • Sirtuin 3 prevents cardiovascular disease by protecting mitochondria. • Sirtuin 3 agonists may become new drugs for cardiovascular diseases.
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