线粒体自噬对急性肾损伤的保护作用  

Protective role of mitophagy in acute kidney injury

作　　者：沈瑞华(综述) 乔晞(审校)[1] SHEN Ruihua;QIAO Xi(Department of Nephrology,Second Hospital of Shanxi Medical University,Shanxi Kidney Disease Institute,Taiyuan 030001,China)

机构地区：[1]山西医科大学第二医院肾内科山西省肾脏病研究所,太原030001

出　　处：《肾脏病与透析肾移植杂志》2022年第4期363-367,共5页Chinese Journal of Nephrology,Dialysis & Transplantation

基　　金：国家自然科学基金面上项目(81970643);山西省回国留学人员科研资助项目(2020-186);山西省留学回国人员科技活动择优资助项目(2017-29)。

摘　　要：近年来,全球范围内急性肾损伤(AKI)的发病率和死亡率增加。线粒体自噬通过清除受损、功能障碍的线粒体,在减少活性氧积累、维持细胞正常能量代谢、抑制炎症反应、维持线粒体动力学稳态等方面具有重要作用。研究表明在缺血再灌注损伤、顺铂、对比剂、脓毒症等诱导的AKI中,线粒体自噬缺陷促进肾小管上皮细胞损伤,导致肾功能下降。本文就线粒体自噬在AKI中的保护作用进行综述,旨在寻找新的治疗靶点,改善AKI患者预后。Acute kidney injury(AKI)is a systemic clinic syndrome increasing morbidity and mortality worldwide in recent years.Mitophagy plays a prominent role in reactive oxygen species elimination,energy metabolism,inhibiting inflammation,and mitochondrial dynamics hemostasis by engulfing injured and dysfunctional mitochondria.Experimental studies have shown that mitophagy deficiency promotes renal tubular epithelial damage and renal function decreasing in AKI induced by ischemia reperfusion injury,cisplatin,contrast agents and sepsis.The review will introduce the protective role of mitophagy in AKI,which may serve as novel therapeutic targets for the development of potential therapies to improve AKI prognosis.

关 键 词：线粒体自噬 急性肾损伤 活性氧 炎症 

分 类 号：R692[医药卫生—泌尿科学]