线粒体SIRT3在肾缺血再灌注损伤中作用的研究进展

Research advances on role of mitochondrial SIRT3 during renal ischemia-reperfusion injury

摘要: 肾缺血再灌注损伤（renal ischemia-reperfusion injury，RIRI）在临床上具有高发病率和高病死率，目前缺乏有效治疗手段。线粒体损伤是急性肾损伤（acute kidney injury，AKI）最重要的病理生理学表现之一，定位于线粒体的去乙酰化酶沉默信息调节因子3（silence information regulator 3，SIRT3）对于线粒体正常发挥功能、保持结构完整性至关重要，研究发现SIRT3能通过抗氧化应激、恢复线粒体膜通透性、调节线粒体动力学、促进线粒体生物发生等机制减轻RIRI，是治疗RIRI的潜在靶点。本文对近年来相关研究进行回顾，主要就SIRT3的特点及其在RIRI中的作用机制进行阐述。

Abstract: Renal ischemia-reperfusion injury(RIRI) has such a high level of morbidity and mortality so that it lacks any effective treatment. Mitochondrial injury is one of the most important pathophysiological manifestations of acute kidney injury(AKI). Essential for mitochondrial function and structural integrity,mitochondrial deacetylase silence information regulator 3(SIRT3) lessons RIRI through antagonizing oxidative stress,restoring mitochondrial membrane permeability,regulating mitochondrial dynamics and promoting mitochondrial biogenesis. It is a potential therapeutic target for RIRI. This review summarized the relevant researches of RIRI and SIRT3 in recent years.