| Autor: |
Wei Chen, Yilan Shen, Jiajun Fan, Xian Zeng, Xuyao Zhang, Jingyun Luan, Yichen Wang, Jinghui Zhang, Si Fang, Xiaobin Mei, Zhen Zhao, Dianwen Ju |
| Jazyk: |
angličtina |
| Rok vydání: |
2021 |
| Předmět: |
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| Zdroj: |
Clinical and Translational Medicine, Vol 11, Iss 2, Pp n/a-n/a (2021) |
| Druh dokumentu: |
article |
| ISSN: |
2001-1326 |
| DOI: |
10.1002/ctm2.324 |
| Popis: |
Abstract Kidney damage initiates the deteriorating metabolic states in tubule cells that lead to the development of end‐stage renal disease (ESTD). Interleukin‐22 (IL‐22) is an effective therapeutic antidote for kidney injury via promoting kidney recovery, but little is known about the underlying molecular mechanisms. Here, we first provide evidence that IL‐22 attenuates kidney injury via metabolic reprogramming of renal tubular epithelial cells (TECs). Specifically, our data suggest that IL‐22 regulates mitochondrial function and glycolysis in damaged TECs. Further observations indicate that IL‐22 alleviates the accumulation of mitochondrial reactive oxygen species (ROS) and dysfunctional mitochondria via the induction of AMPK/AKT signaling and PFBFK3 activities. In mice, amelioration of kidney injury and necrosis and improvement of kidney functions via regulation of these metabolism relevant signaling and mitochondrial fitness of recombinant IL‐22 are certificated in cisplatin‐induced kidney damage and diabetic nephropathy (DN) animal models. Taken together, our findings unravel new mechanistic insights into protective effects of IL‐22 on kidneys and highlight the therapeutic opportunities of IL‐22 and the involved metabolic regulators in various kidney diseases. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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