{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["8"],"submitter":["Yu L"],"funding":["National Natural Science Foundation of China","Science and Technology Department, Henan Province"],"pubmed_abstract":["It is well-established that mitophagy leads to Diabetic Nephropathy (DN) and renal failure. Mitophagy mediated by a Hypoxia-inducible factor-1α (HIF-1α) plays a beneficial role in many diseases. Nevertheless, the mechanisms underlying HIF-1α-mediated mitophagy in DN remain unclear. This study defines the role of HIF-1α mediated mitophagy in DN. The expression of HIF-1α was upregulated in HK-2 cells in an High-Glucose (HG) environment, and the YC-1 (a specific inhibitor of HIF-1α) further exacerbated the hypoxia-induced mitochondrial dysfunction. Conversely, the HIF-1α-mediated protective effect was strengthened by scavenger N-acetylcysteine (NAC), a type of reactive oxygen species. Moreover, HIF-1α-Parkin/PINK1-mediated mitophagy prevented apoptosis and ROS production in HK-2 cells subject"],"journal":["Frontiers in medicine"],"pagination":["803874"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8850720"],"repository":["biostudies-literature"],"pubmed_title":["HIF-1α Alleviates High-Glucose-Induced Renal Tubular Cell Injury by Promoting Parkin/PINK1-Mediated Mitophagy."],"pmcid":["PMC8850720"],"pubmed_authors":["Yu L","Yang Z","Tang L","Guo YH","Zhai ZH","Wang Y","Wang L"],"additional_accession":[]},"is_claimable":false,"name":"HIF-1α Alleviates High-Glucose-Induced Renal Tubular Cell Injury by Promoting Parkin/PINK1-Mediated Mitophagy.","description":"It is well-established that mitophagy leads to Diabetic Nephropathy (DN) and renal failure. Mitophagy mediated by a Hypoxia-inducible factor-1α (HIF-1α) plays a beneficial role in many diseases. Nevertheless, the mechanisms underlying HIF-1α-mediated mitophagy in DN remain unclear. This study defines the role of HIF-1α mediated mitophagy in DN. The expression of HIF-1α was upregulated in HK-2 cells in an High-Glucose (HG) environment, and the YC-1 (a specific inhibitor of HIF-1α) further exacerbated the hypoxia-induced mitochondrial dysfunction. Conversely, the HIF-1α-mediated protective effect was strengthened by scavenger N-acetylcysteine (NAC), a type of reactive oxygen species. Moreover, HIF-1α-Parkin/PINK1-mediated mitophagy prevented apoptosis and ROS production in HK-2 cells subject","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021","modification":"2025-04-21T23:14:38.956Z","creation":"2025-04-05T19:05:06.288Z"},"accession":"S-EPMC8850720","cross_references":{"pubmed":["35186974"],"doi":["10.3389/fmed.2021.803874"]}}