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作 者:Yu Xiang Ying Fu Wenwen Wu Chengyuan Tang Zheng Dong
机构地区:[1]Department of Nephrology,Hunan Key Laboratory of Kidney Disease and Blood Purification,The Second Xiangya Hospital at Central South University,Changsha 410000,Hunan Province,China [2]Department of Cellular Biology and Anatomy,Medical College of Georgia at Augusta University and Charlie Norwood VA Medical Center,Augusta,GA 30912,USA
出 处:《Burns & Trauma》2023年第1期146-154,共9页烧伤与创伤(英文)
基 金:supported partly by grants from the National Natural Science Foundation of China(81720108008,82090024);the National Key R&D Program of China(2020YFC2005000).
摘 要:Acute kidney injury(AKI)is a major renal disease characterized by a sudden decrease in kidney function.After AKI,the kidney has the ability to repair,but if the initial injury is severe the repair may be incomplete or maladaptive and result in chronic kidney problems.Autophagy is a highly conserved pathway to deliver intracellular contents to lysosomes for degradation.Autophagy plays an important role in maintaining renal function and is involved in the pathogenesis of renal diseases.Autophagy is activated in various forms of AKI and acts as a defense mechanism against kidney cell injury and death.After AKI,autophagy is maintained at a relatively high level in kidney tubule cells during maladaptive kidney repair but the role of autophagy in maladaptive kidney repair has been controversial.Nonetheless,recent studies have demonstrated that autophagy may contribute to maladaptive kidney repair after AKI by inducing tubular degeneration and promoting a profibrotic phenotype in renal tubule cells.In this review,we analyze the role and regulation of autophagy in kidney injury and repair and discuss the therapeutic strategies by targeting autophagy.
关 键 词:AUTOPHAGY Acute kidney injury Maladaptive repair FIBROSIS Chronic kidney disease
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