SIRT3：心血管疾病的新调控因子。
SIRT3: A New Regulator of Cardiovascular Diseases.
机构信息
Department of Cardiology, The Second Hospital of Jilin University, 218 Ziqiang Road, Changchun 130041, China.
Department of Neurology, The Liaoning Province People's Hospital, 33 Wenyi Road, Shenyang 110016, China.
出版信息
Oxid Med Cell Longev. 2018 Feb 13;2018:7293861. doi: 10.1155/2018/7293861. eCollection 2018.
Abstract
Cardiovascular diseases (CVDs) are the leading causes of death worldwide, and defects in mitochondrial function contribute largely to the occurrence of CVDs. Recent studies suggest that sirtuin 3 (SIRT3), the mitochondrial NAD-dependent deacetylase, may regulate mitochondrial function and biosynthetic pathways such as glucose and fatty acid metabolism and the tricarboxylic acid (TCA) cycle, oxidative stress, and apoptosis by reversible protein lysine deacetylation. SIRT3 regulates glucose and lipid metabolism and maintains myocardial ATP levels, which protects the heart from metabolic disturbances. SIRT3 can also protect cardiomyocytes from oxidative stress-mediated cell damage and block the development of cardiac hypertrophy. Recent reports show that SIRT3 is involved in the protection of several heart diseases. This review discusses the progress in SIRT3-related research and the role of SIRT3 in the prevention and treatment of CVDs.
摘要
心血管疾病（CVDs）是全球范围内主要的死亡原因，线粒体功能缺陷在 CVDs 的发生中起着重要作用。最近的研究表明，线粒体 NAD 依赖性去乙酰化酶 SIRT3（sirtuin 3）可能通过可逆的蛋白赖氨酸去乙酰化来调节线粒体功能和生物合成途径，如葡萄糖和脂肪酸代谢以及三羧酸（TCA）循环、氧化应激和细胞凋亡。SIRT3 调节葡萄糖和脂质代谢并维持心肌 ATP 水平，从而保护心脏免受代谢紊乱的影响。SIRT3 还可以保护心肌细胞免受氧化应激介导的细胞损伤，并阻止心脏肥大的发展。最近的报告表明，SIRT3 参与了多种心脏病的保护。本文综述了 SIRT3 相关研究的进展以及 SIRT3 在 CVDs 的预防和治疗中的作用。
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