Sirt3 modulates fatty acid oxidation and attenuates cisplatin‐induced AKI in mice
| العنوان: | Sirt3 modulates fatty acid oxidation and attenuates cisplatin‐induced AKI in mice |
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| المؤلفون: | Hui Peng, Tanqi Lou, Ming Li, Jia-Yan Huang, Weiyan Lai, Can-Ming Li, Zengchun Ye, Yin Li |
| المصدر: | Journal of Cellular and Molecular Medicine |
| بيانات النشر: | Wiley, 2020. |
| سنة النشر: | 2020 |
| مصطلحات موضوعية: | Male, 0301 basic medicine, cisplatin, Apoptosis, Fatty Acids, Nonesterified, Mitochondrion, Pharmacology, Kidney Function Tests, Lipid peroxidation, Mice, chemistry.chemical_compound, 0302 clinical medicine, Sirtuin 3, mitochondrion, Phosphorylation, Beta oxidation, fatty acid oxidation, Mice, Knockout, chemistry.chemical_classification, Kidney, biology, Fatty Acids, digestive, oral, and skin physiology, Acute kidney injury, food and beverages, Acetylation, Acute Kidney Injury, Prognosis, Lipids, Mitochondria, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Sirtuin, Molecular Medicine, Original Article, SIRT3, Antineoplastic Agents, Lignans, 03 medical and health sciences, medicine, Sirtuin3, Animals, Metabolomics, Biphenyl Compounds, Fatty acid, Original Articles, Cell Biology, Lipid Metabolism, medicine.disease, 030104 developmental biology, chemistry, biology.protein, Lipid Peroxidation, Reactive Oxygen Species |
| الوصف: | Fatty acid oxidation (FAO) dysfunction is one of the important mechanisms of renal fibrosis. Sirtuin 3 (Sirt3) has been confirmed to alleviate acute kidney injury (AKI) by improving mitochondrial function and participate in the regulation of FAO in other disease models. However, it is not clear whether Sirt3 is involved in regulating FAO to improve the prognosis of AKI induced by cisplatin. Here, using a murine model of cisplatin‐induced AKI, we revealed that there were significantly FAO dysfunction and extensive lipid deposition in the mice with AKI. Metabolomics analysis suggested reprogrammed energy metabolism and decreased ATP production. In addition, fatty acid deposition can increase reactive oxygen species (ROS) production and induce apoptosis. Our data suggested that Sirt3 deletion aggravated FAO dysfunction, resulting in increased apoptosis of kidney tissues and aggravated renal injury. The activation of Sirt3 by honokiol could improve FAO and renal function and reduced fatty acid deposition in wide‐type mice, but not Sirt3‐defective mice. We concluded that Sirt3 may regulate FAO by deacetylating liver kinase B1 and activating AMP‐activated protein kinase. Also, the activation of Sirt3 by honokiol increased ATP production as well as reduced ROS and lipid peroxidation through improving mitochondrial function. Collectively, these results provide new evidence that Sirt3 is protective against AKI. Enhancing Sirt3 to improve FAO may be a potential strategy to prevent kidney injury in the future. |
| تدمد: | 1582-4934 1582-1838 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a741316cf53d53be1e3ef9b79d90ecd4Test https://doi.org/10.1111/jcmm.15148Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....a741316cf53d53be1e3ef9b79d90ecd4 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15824934 15821838 |
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