丁晓青1 , 马春伟1 , 高炳宏2,*
1上海体育学院运动科学学院,上海 200438 2上海体育学院体育教育训练学院,上海 200438

摘 要:

线粒体自噬是一种选择性清除多余或受损线粒体的过程,在调节细胞内线粒体质量和维持线粒体能量代谢等方面发挥重要作用。SIRT3 是一种定位于线粒体的组蛋白去乙酰化酶,参与多种细胞调节过程。近年来相关研究发现SIRT3 可调节病理性心肌PINK1/Parkin、p62 以及BNIP3、FUNDC1 等相关蛋白表达,参与自噬体的形成,调控线粒体自噬过程。本文对SIRT3 调控病理性心肌线粒体自噬的相关机制及相关临床应用进行总结,为心肌线粒体自噬异常的相关心肌疾病提供新的研究靶点和治疗方案。


通讯作者:高炳宏 ,

Advances in SIRT3-regulated pathological myocardial mitophagy
DING Xiao-Qing1 , MA Chun-Wei1 , GAO Bing-Hong2,*
1School of Kinesiology, Shanghai University of Sport, Shanghai 200438, China 2School of Sports Education and Training, Shanghai University of Sport, Shanghai 200438, China


Mitophagy is a process that selectively removes excess or damaged mitochondria and plays an important role in regulating intracellular mitochondrial mass and maintaining mitochondrial energy metabolism. SIRT3 is a histone deacetylase localized in mitochondria and is involved in various cellular regulatory processes. Recent studies have found that SIRT3 can regulate the expression of related proteins such as PINK1/Parkin, P62, BNIP3 and FUNDC1 in pathological myocardium, and participate in the formation of autophagosomes and regulate the process of mitophagy. This review summarizes the mechanisms related to the regulation of mitophagy in pathological myocardium by SIRT3 and related clinical applications to provide new research targets and therapeutic options for myocardial diseases associated with abnormal myocardial mitophagy.

Communication Author:GAO Bing-Hong ,

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