琥珀酰化
氧化应激
锡尔图因
线粒体
再灌注损伤
氧化磷酸化
化学
生物化学
缺血
医学
内科学
乙酰化
基因
作者
Yan Hu,Xinyao Tian,Yan Zhao,Zhecheng Wang,Musen Lin,Ruimin Sun,Yue Wang,Zhanyu Wang,Guiru Li,Shusen Zheng,Jihong Yao
标识
DOI:10.1089/ars.2022.0137
摘要
Mitochondrial dysfunction is the primary mechanism of liver ischemia/reperfusion (I/R) injury. The lysine desuccinylase sirtuin 5 (SIRT5) is a global regulator of the mitochondrial succinylome and has pivotal roles in mitochondrial metabolism and function; however, its hepatoprotective capacity in liver I/R remains unclear. In this study, we established liver I/R model in SIRT5-silenced and SIRT5-overexpressed mice to examine the role and precise mechanisms of SIRT5 in liver I/R injury.
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