SIRT3调控线粒体蛋白去乙酰化参与心肌保护  

SIRT3 involved in protecting heart by regulating mitochondrial protein deacetylation

作　　者：孙宇[1] 刘宁[1] 张林雪[1] 张伟华[1] 

机构地区：[1]哈尔滨医科大学病理生理学教研室,黑龙江哈尔滨150080

出　　处：《解剖科学进展》2017年第2期212-215,217,共5页Progress of Anatomical Sciences

基　　金：国家自然科学基金(81670344;81370421;81370330)

摘　　要：Sirtuins是一类NAD^+依赖性组蛋白去乙酰化酶,包括7个成员(SIRT1~SIRT7),每个成员都有不同的细胞定位并且发挥不同的生物学功能。SIRT3通过对线粒体蛋白质赖氨酸的去乙酰化修饰,调控线粒体功能和生物合成,如糖脂代谢、三羧酸循环、氧化应激以及凋亡等。SIRT3通过调节糖脂代谢过程维持心肌ATP水平而保护由于代谢紊乱造成的心肌损伤,SIRT3还可以在氧化应激造成的心肌损伤中保护心脏以及阻止心肌肥大的发生。Sirtuins, a family of nicotinamide adenine dinucleotide（NAD＋）-dependent protein deacetylascs, contain seven sirtuin analogues（SIRT1 to SIRT7）, with distinct subcellular locations and biological functions. As a major mitochondrial deacetylase, SIRT3 can modulate mitochondrial function and biosynthesis by deacetylation of the targeted lysine on the mitochondrial protein, such as glucose and fatty acid metabolism, TCA cycle, oxidative stress and apoptosis. SIRT3 was found to regulate glucose and lipid metabolism and maintenance of myocardial ATP levels to protect heart from metabolic disturbance. SIRT3 can also protect cardiomyocytes from oxidative stress-mediated cell damage and block the development of cardiac hypertrophy.

关 键 词：去乙酰化 SIRT3 心肌保护 糖脂代谢 三羧酸循环 氧化应激 心肌肥大 线粒体蛋白 肌损伤 生物合成 

分 类 号：R542.2[医药卫生—心血管疾病]