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Targeting Sirtuin1 to treat aging-related tissue fibrosis: From prevention to therapy
Pharmacology & Therapeutics ( IF 13.5 ) Pub Date : 2021-09-02 , DOI: 10.1016/j.pharmthera.2021.107983
Xin Han 1 , Chuan Ding 1 , XiaNan Sang 1 , MengYun Peng 1 , Qiao Yang 1 , Yan Ning 1 , Qiang Lv 1 , QiYuan Shan 1 , Min Hao 1 , KuiLong Wang 1 , Xin Wu 1 , Hongyan Zhang 2 , Gang Cao 1
Affiliation  

Fibrosis, which is characterized by excessive extracellular matrix (ECM) deposition, is a wound-healing response to organ injury and may promote cancer and failure in various organs, such as the heart, liver, lung, and kidney. Aging associated with oxidative stress and inflammation exacerbates cellular dysfunction, tissue failure, and body function disorders, all of which are closely related to fibrosis. Sirtuin-1 (SIRT1) is a class III histone deacetylase that regulates growth, transcription, aging, and metabolism in various organs. This protein is downregulated in organ injury and fibrosis associated with aging. Its expression and distribution change with age in different organs and play critical roles in tissue oxidative stress and inflammation. This review first described the background on fibrosis and regulatory functions of SIRT1. Second, we summarized the relationships of SIRT1 with other proteins and its protective action during fibrosis in the heart, liver, lung and kidney. Third, the activation of SIRT1 in therapies of tissue fibrosis, especially in liver fibrosis and aging-related tissue injury, was analyzed. In conclusion, SIRT1 targeting may be a new therapeutic strategy in fibrosis.



中文翻译:

靶向 Sirtuin1 治疗衰老相关组织纤维化:从预防到治疗

纤维化的特征是过度的细胞外基质 (ECM) 沉积,是一种对器官损伤的伤口愈合反应,可能会促进各种器官(如心脏、肝脏、肺和肾脏)的癌症和衰竭。与氧化应激和炎症相关的衰老会加剧细胞功能障碍、组织衰竭和身体功能障碍,所有这些都与纤维化密切相关。Sirtuin-1 (SIRT1) 是一种 III 类组蛋白脱乙酰酶,可调节各种器官的生长、转录、衰老和新陈代谢。这种蛋白质在与衰老相关的器官损伤和纤维化中被下调。它在不同器官中的表达和分布随着年龄的增长而变化,并在组织氧化应激和炎症中起关键作用。本综述首先描述了 SIRT1 的纤维化背景和调控功能。第二,我们总结了 SIRT1 与其他蛋白质的关系及其在心脏、肝脏、肺和肾脏纤维化过程中的保护作用。第三,分析了 SIRT1 在组织纤维化治疗中的激活,特别是在肝纤维化和衰老相关组织损伤中的作用。总之,SIRT1靶向可能是一种新的纤维化治疗策略。

更新日期:2021-09-02
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