<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>8</volume><submitter>Yu L</submitter><funding>National Natural Science Foundation of China</funding><funding>Science and Technology Department, Henan Province</funding><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</pubmed_abstract><journal>Frontiers in medicine</journal><pagination>803874</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8850720</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>HIF-1α Alleviates High-Glucose-Induced Renal Tubular Cell Injury by Promoting Parkin/PINK1-Mediated Mitophagy.</pubmed_title><pmcid>PMC8850720</pmcid><pubmed_authors>Yu L</pubmed_authors><pubmed_authors>Yang Z</pubmed_authors><pubmed_authors>Tang L</pubmed_authors><pubmed_authors>Guo YH</pubmed_authors><pubmed_authors>Zhai ZH</pubmed_authors><pubmed_authors>Wang Y</pubmed_authors><pubmed_authors>Wang L</pubmed_authors></additional><is_claimable>false</is_claimable><name>HIF-1α Alleviates High-Glucose-Induced Renal Tubular Cell Injury by Promoting Parkin/PINK1-Mediated Mitophagy.</name><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</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021</publication><modification>2025-04-21T23:14:38.956Z</modification><creation>2025-04-05T19:05:06.288Z</creation></dates><accession>S-EPMC8850720</accession><cross_references><pubmed>35186974</pubmed><doi>10.3389/fmed.2021.803874</doi></cross_references></HashMap>