Gong Li, Pan Qingjun, Yang Nianlan
Experimental Animal Center, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Institute of Nephrology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Front Physiol. 2020 Sep 25;11:576463. doi: 10.3389/fphys.2020.576463. eCollection 2020.
Autophagy at an appropriate juncture in the cell cycle exerts protective effects in acute kidney injury (AKI), whereas abnormal autophagy may lead to cell death. Inflammatory response plays a pivotal role in the pathophysiological process of kidney injury and repair during AKI. Several studies have reported an interaction between autophagy and inflammation in the pathogenesis of AKI. This review outlines recent advances in the investigation of the role of autophagy in inflammatory response regulation based on the following aspects. (1) Autophagy inhibits inflammatory responses induced in AKI through the regulation of mTOR and AMPK pathways and the inhibition of inflammasomes activation. (2) Autophagy can also help in the regulation of inflammatory responses through the nuclear factor kappa B pathway, which is beneficial to the recovery of kidney tissues. These studies reviewed here provide better insight into the mechanisms underlying the protective effects of the autophagy-inflammatory pathway. Through this review, we suggest that the autophagy-inflammatory pathway may serve as an alternative target for the treatment of AKI.
在细胞周期的适当阶段进行自噬对急性肾损伤(AKI)具有保护作用,而异常自噬可能导致细胞死亡。炎症反应在AKI期间肾脏损伤和修复的病理生理过程中起关键作用。几项研究报告了自噬与炎症在AKI发病机制中的相互作用。本综述基于以下几个方面概述了自噬在炎症反应调节中作用的研究进展。(1)自噬通过调节mTOR和AMPK途径以及抑制炎性小体激活来抑制AKI中诱导的炎症反应。(2)自噬还可以通过核因子κB途径帮助调节炎症反应,这有利于肾组织的恢复。此处综述的这些研究为自噬-炎症途径保护作用的潜在机制提供了更好的见解。通过本综述,我们认为自噬-炎症途径可能成为治疗AKI的替代靶点。