Autophagy and Acute Kidney Injury

被引:14
|
作者
Cui, Jing [1 ]
Bai, Xueyuan [1 ]
Chen, Xiangmei [1 ]
机构
[1] Chinese Peoples Liberat Army Gen Hosp, Natl Clin Res Ctr Kidney Dis, Chinese PLA Inst Nephrol,Dept Nephrol, State Key Lab Kidney Dis,Beijing Key Lab Kidney D, Beijing, Peoples R China
关键词
Reactive oxygen species; Autophagy; Acute kidney injury; Ischemia-reperfusion; CELL-DEATH; APOPTOSIS;
D O I
10.1007/978-981-15-4272-5_34
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Acute kidney injury (AKI) is one of the major kidney diseases associated with poor clinical outcomes both in short- and long-term, which caused by toxins, transient ischemia, and so on. Autophagy is a cellular stress response that plays important roles in the pathogenesis of various diseases, including kidney diseases. Autophagy is induced in proximal tubules during AKI. It has been demonstrated that autophagy plays a renoprotective role in AKI by pharmacological and genetic inhibitory studies. However, the role of autophagy in kidney recovery and repair from AKI remains unknown mostly. In many studies, a dynamic change of autophagy was important for tubular proliferation and repair in the recovery phase of AKI. Moreover, autophagy may not only promote renal fibrosis through inducing tubular atrophy and decomposition but also prevent it by mediating intracellular degradation of excessive collagen in terms of renal fibrosis. In further researches, we expect to clarify the regulation of autophagy in kidney injury and repair, and find out therapeutic drugs for treating AKI and preventing its progression to chronic kidney disease.
引用
收藏
页码:469 / 480
页数:12
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