SIRT3
氧化应激
血管紧张素II
线粒体
下调和上调
上皮-间质转换
调解人
癌症研究
细胞生物学
生物
内分泌学
化学
锡尔图因
生物化学
乙酰化
血压
基因
作者
Ping He,Zhuoming Li,Zhongbao Yue,Hui Gao,Guoshuai Feng,Panxia Wang,Yi Huang,Wenwei Luo,HuiQi Hong,Liang Liu,Shao‐Rui Chen,Peiqing Liu
标识
DOI:10.1016/j.mce.2017.04.027
摘要
Silent mating type information regulation 2 homolog 3 (SIRT3) is a major protective mediator that ameliorates oxidative stress and mitochondrial dysfunction, which are associated with the pathogenesis of epithelial-mesenchymal transition (EMT). The present study was aimed to investigate the potential role of SIRT3 in renal tubular EMT both in vitro and in vivo. Firstly, we showed that the expression of SIRT3 was repressed in angiotensin II-induced EMT. SIRT3 deficiency triggered EMT response, while over-expression of SIRT3 attenuated EMT response. In addition, over-expression of SIRT3 repressed AngⅡ-induced excessive production of mitochondrial superoxide, as well as mitochondrial dysfunction evidenced by the maintenance of mitochondrial number and morphology, and the stabilization of mitochondrial membrane potential. In conclusion, these findings identify a protective role of SIRT3 against angiotensin II-induced EMT in the kidney, and suggest SIRT3 upregulation is a potential therapeutic strategy for the treatment of renal tubulointerstitial fibrosis.
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