Basic & Clinical Medicine ›› 2022, Vol. 42 ›› Issue (11): 1799-1803.doi: 10.16352/j.issn.1001-6325.2022.10.1799

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Research progress on the role of mitochondrial SIRT3 in organ fibrosis

QI Jun-qing1, CAO Meng-fei2, ZHAO Qian-ru2, YIN Jun3*   

  1. 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

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

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