Relieving lipid accumulation through UCP1 suppresses the progression of acute kidney injury by promoting the AMPK/ULK1/autophagy pathway
| Autor: | Wei Xiong, Anni Song, Chen Ye, Chun Zhang, Chun-Tao Lei, Zhiyong Xiong |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
UCP1 autophagy Cell Medicine (miscellaneous) urologic and male genital diseases lipids 03 medical and health sciences Mice 0302 clinical medicine Western blot medicine metabolic reprogramming Animals Autophagy-Related Protein-1 Homolog Pharmacology Toxicology and Pharmaceutics (miscellaneous) Triglycerides Uncoupling Protein 1 medicine.diagnostic_test business.industry urogenital system Autophagy Adenylate Kinase Acute kidney injury AMPK Lipid metabolism ULK1 Acute Kidney Injury medicine.disease Lipid Metabolism Thermogenin female genital diseases and pregnancy complications Up-Regulation 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis Lipidomics Cancer research Disease Progression business Research Paper |
| Zdroj: | Theranostics |
| ISSN: | 1838-7640 |
| Popis: | Rationale: Acute kidney injury (AKI) is a serious clinical emergency with an acute onset, rapid progression, and poor prognosis. Recent evidence suggests that AKI is accompanied by significant metabolic abnormalities, including alterations in lipid metabolism. However, the specific changes in lipids in AKI, and their role and regulation mechanisms are currently unclear. Methods: Quantitative metabolomics was performed in AKI models to reveal the differences of lipid metabolism-related products. Regulated pathway was detected by western blot, qRT-PCR, immunoblot analysis and immunohistochemistry. Results: The present study systematically analyzes the changes in lipid composition in AKI for the first time and find that the degree of lipid accumulation was highly correlated with uncoupling protein 1 (UCP1). Importantly, relieving lipid accumulation in AKI by upregulating UCP1 can significantly inhibit the progression of AKI through promoting AMPK/ULK1/autophagy pathway. Conclusions: The present findings suggest that lipid accumulation in AKI is directly regulated by UCP1, which can activate cell autophagy and thus significantly inhibit disease progression. It will provide new ideas and targets for the treatment of AKI. |
| Databáze: | OpenAIRE |
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