摘要
急性肾损伤(acute kidney injury,AKI)是一种具有全身效应的临床综合征,特征为肾小球滤过率急剧下降,其发病率高,病死率高。然而AKI的发病机制目前尚不清楚,但线粒体功能障碍在其进展过程中起着重要作用。线粒体靶蛋白的主要脱乙酰酶沉默信息调节因子3(silence information regulator 3,SIRT3)通过调节线粒体生物合成、改善线粒体动力学、诱导线粒体自噬以及减少氧化应激维持线粒体稳态来改善AKI。在本综述中,我们阐述了SIRT3介导的线粒体稳态在AKI中的作用机制,对于治疗AKI以及改善患者预后的意义重大。
As a clinical syndrome with systemic manifestations,acute kidney injury(AKI)is char-acterized by a sharp decline in glomerular filtration rate,high morbidity and mortality.However,the patho-genesis of AKI has remained elusive.Mitochondrial dysfunction plays an important role in its progression.And silence information regulator 3(SIRT3),a major deacetylase regulator of mitochondrial target pro-teins,ameliorates AKI through regulating mitochondrial biosynthesis,improving mitochondrial dynamics,inducing mitochondrial autophagy and reducing oxidative stress to maintain mitochondrial homeostasis.Elucidating the underlying mechanism of SIRT3-mediated mitochondrial homeostasis in AKI is of great significance for managing AKI and improving patient outcomes.
作者
李鹏艳
杨定平
Li Peng-yan;Yang Ding-ping(Department of Nephrology,Renmin Hospital of Wuhan University,Wuhan 430060,China)
出处
《临床肾脏病杂志》
2024年第4期329-334,共6页
Journal Of Clinical Nephrology
基金
国家自然科学基金(81670631)。
关键词
急性肾损伤
线粒体
沉默信息调节因子
Acute kidney injury
Mitochondrion
Silence infor-mation regulator
作者简介
通信作者:杨定平,Email:shenbinneike@163.com。
