《生命科学》 2023, 35(8): 1080-10188

SIRT3在纤维化疾病中的研究进展

许雅萍¹ , 王语涵¹ , 李　南¹ , 陈婷婷¹ , 魏　伟¹ , 王　华^2,* , 孙妩弋^1,*

¹安徽医科大学临床药理研究所，抗炎免疫药物教育部重点实验室， 合肥 230032 ²安徽医科大学第一附属医院肿瘤科，合肥 230032

摘　要：

纤维化是大多数慢性炎症性疾病的病理特征，临床中较常见的包括肝纤维化、肾纤维化、心肌纤维化和肺纤维化等。持续发展的纤维化可破坏组织正常结构并影响其功能，甚至引起器官衰竭和死亡，目前尚无有效治疗策略。沉默信息调节因子3 (sirtuin3, SIRT3) 是一种线粒体去乙酰化酶，已被证明参与线粒体代谢和体内平衡的多个方面，保护线粒体免受各种损伤。近年来相关研究发现，SIRT3 在心脏、肝、肾、肺等多种器官纤维化中均有不同程度的表达，通过调节线粒体代谢、细胞凋亡、自噬等生物过程，参与纤维化的发生发展。本文就SIRT3 在纤维化疾病中的调控作用进行综述。

通讯作者：王　华 , Email:wanghua@ahmu.edu.cn 孙妩弋 , Email:sunwuyi51@aliyun.com

Advances of SIRT3 in fibrotic diseases

XU Ya-Ping¹ , WANG Yu-Han¹ , LI Nan¹ , CHEN Ting-Ting¹ , WEI Wei¹ , WANG Hua^2,* , SUN Wu-Yi^1,*

¹Key Laboratory of Anti-inflammatory and Immune Drugs, Ministry of Education, Institute of Clinical Pharmacology, Anhui Medical University, Hefei 230032, China ²Department of Oncology, the First Affiliated Hospital of Anhui Medical University, Hefei 230032, China

Abstract:

Fibrosis is the pathological feature of most chronic inflammatory diseases, including liver fibrosis, renal fibrosis, myocardial fibrosis, and pulmonary fibrosis. The continuous development of fibrosis can destroy the normal structure of tissue and affect its function, even causing organ failure and death, but there is no effective treatment strategy at present. Sirtuin3 (SIRT3) is a mitochondrial deacetylase, which has been proven to participate in many aspects of mitochondrial metabolism and homeostasis and protect mitochondria from various damages. Recent studies have found that SIRT3 is expressed to varying degrees in various organ fibrosis, such as the heart, liver, kidney, and lung. It participates in the occurrence and development of fibrosis by regulating biological processes such as mitochondrial metabolism, cell apoptosis, and autophagy. This article reviews the regulatory role of SIRT3 in fibrosis.

Communication Author：WANG Hua , Email:wanghua@ahmu.edu.cn SUN Wu-Yi , Email:sunwuyi51@aliyun.com