线粒体SIRT3在器官纤维化中作用的研究进展

doi:10.16352/j.issn.1001-6325.2022.10.1799

基础医学与临床 ›› 2022, Vol. 42 ›› Issue (11): 1799-1803.doi: 10.16352/j.issn.1001-6325.2022.10.1799

线粒体SIRT3在器官纤维化中作用的研究进展

祁俊清¹, 曹梦菲², 赵倩茹², 尹俊^3*

1.江苏大学附属人民医院心胸外科, 江苏镇江 212002;
2.江苏大学附属医院心内科, 江苏镇江 212001;
3.复旦大学附属中山医院胸外科, 上海 200032

收稿日期:2022-04-27 修回日期:2022-07-21 出版日期:2022-11-05 发布日期:2022-11-01
通讯作者: ^* yin912@126.com

Research progress on the role of mitochondrial SIRT3 in organ fibrosis

QI Jun-qing¹, CAO Meng-fei², ZHAO Qian-ru², YIN Jun^3*

1. Department of Cardiothoracic Surgery, People's Hospital of Jiangsu University, Zhenjiang 212002;
2. Department of Cardiology, the Affiliated Hospital of Jiangsu University, Zhenjiang 212001;
3. Department of Thoracic Surgery, Zhongshan Hospital of Fudan University, Shanghai 200032, China

Received:2022-04-27 Revised:2022-07-21 Online:2022-11-05 Published:2022-11-01
Contact: ^* yin912@126.com

摘要/Abstract

摘要： 器官纤维化是造成脏器功能障碍的主要原因,且目前尚缺乏有效应用于临床治疗的抗纤维化疗法。而SIRT3作为一种重要的线粒体去乙酰化酶,可通过调节线粒体蛋白乙酰化水平保护线粒体免受各种损伤,从而在器官纤维化中发挥作用。SIRT3能通过调节线粒体代谢、氧化应激、线粒体动力学等方面减缓或抑制器官纤维化的进程。

关键词: SIRT3, 线粒体, 去乙酰化酶, 纤维化

Abstract: Organ fibrosis is the main cause of organ dysfunction, and there is no effective anti-fibrosis clinical therapy yet. SIRT3 is an important mitochondrial deacetylase that plays a role in organ fibrosis by regulating mitochondrial protein acetylation level to protect mitochondria from various types of damage. SIRT3 can retard or inhibit the process of organ fibrosis by regulating mitochondrial metabolism, oxidative stress, mitochondrial dynamics, mitochondrial DNA damage, autophagy and apoptosis.

Key words: SIRT3, mitochondrion, deacetylase, fibrosis

中图分类号:

祁俊清, 曹梦菲, 赵倩茹, 尹俊. 线粒体SIRT3在器官纤维化中作用的研究进展[J]. 基础医学与临床, 2022, 42(11): 1799-1803.

QI Jun-qing, CAO Meng-fei, ZHAO Qian-ru, YIN Jun. Research progress on the role of mitochondrial SIRT3 in organ fibrosis[J]. Basic & Clinical Medicine, 2022, 42(11): 1799-1803.

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线粒体SIRT3在器官纤维化中作用的研究进展

Research progress on the role of mitochondrial SIRT3 in organ fibrosis

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