Sestrin-2 regulates podocyte mitochondrial dysfunction and apoptosis under high-glucose conditions via AMPK
| Autor: | Wei Liang, Yanqin Fan, Zhaowei Chen, Guohua Ding, Jijia Hu, Yiqiong Ma, Cheng Chen, Qiaoxuan Lin |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Male Mitochondrial Diseases Apoptosis AMP-Activated Protein Kinases Podocyte Rats Sprague-Dawley 0302 clinical medicine Phosphorylation Cells Cultured Nuclear Proteins General Medicine Articles Middle Aged Mitochondria Up-Regulation medicine.anatomical_structure 030220 oncology & carcinogenesis Female Signal Transduction Adult medicine.medical_specialty Diabetes Mellitus Experimental 03 medical and health sciences Downregulation and upregulation Internal medicine Diabetes mellitus mitochondrial dysfunction Genetics medicine Animals Humans Protein kinase A sestrin-2 Aged Oncogene AMP-activated protein kinase business.industry AMPK medicine.disease diabetic kidney disease Rats 030104 developmental biology Endocrinology Glucose podocytes business Reactive Oxygen Species |
| Zdroj: | International Journal of Molecular Medicine |
| ISSN: | 1791-244X 1107-3756 |
| Popis: | Diabetic kidney disease (DKD) is a severe form of microangiopathy among diabetic patients, of which podocyte injury is one of the more predominant features. There is increasing evidence to suggest that mitochondrial dysfunction is associated with podocyte injury, thus contributing to the progression of DKD. Initially identified as a p53 target protein, the endogenous antioxidant protein, sestrin‑2 (sesn2), has recently attracted attention due to its potential function in various inflammatory diseases. However, the association between sesn2 and podocytes in DKD remains unclear. In the present study, to elucidate the role of sesn2 in podocyte mitochondrial dysfunction, the effects of sesn2 on the regulation of AMP‑activated protein kinase (AMPK) were examined in vitro and in vivo. Abnormal mitochondria were found in rats with streptozotocin‑induced diabetes, and hyperglycemia downregulated the expression of sesn2. The upregulation of sesn2 increased the level of AMPK phosphorylation, and thus ameliorated mitochondrial dysfunction under high glucose conditions (HG). On the whole, these results suggest that sesn2 is associated with mitochondrial dysfunction in podocytes under HG conditions. In addition, the decreased expression of sesn2 may be a therapeutic target for DKD. |
| Databáze: | OpenAIRE |
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