<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhang L</submitter><funding>Beijing Hospitals Authority's Ascent Plan</funding><funding>High-Level Public Health Technical Talent Building Program</funding><funding>National Natural Science Foundation of China</funding><funding>Capital's Funds for Health Improvement and Research</funding><pagination>4607</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11806084</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(1)</volume><pubmed_abstract>Post-cardiac arrest brain injury (PCABI), as the main cause of high mortality and long-term disability in patients, induces mitochondrial damage and cell apoptosis. Hypothermia is well-known as an effective neuroprotective therapy, but its underlying mechanisms deserve further exploration. Previous study has demonstrated that hypothermia provides neuroprotection via increasing PINK1/Parkin-mediated mitophagy. However, whether hypothermia can regulate both apoptosis and mitophagy through the PINK1/Parkin-VDAC3 signaling pathway or not. In this study, BV2 mouse microglial cells were cultured under oxygen-glucose deprivation for 6 h following reperfusion with or without hypothermia for 2-4 h. Cell viability was examined by trypan blue stain. Mitophagy was observed by transmission electron mic</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>Hypothermia regulates mitophagy and apoptosis via PINK1/Parkin-VDAC 3 signaling pathway during oxygen-glucose deprivation/recovery injury.</pubmed_title><pmcid>PMC11806084</pmcid><funding_grant_id>82072136</funding_grant_id><funding_grant_id>CFH 2022-1-2032</funding_grant_id><funding_grant_id>Discipline Leader-01-01</funding_grant_id><funding_grant_id>DFL20240302</funding_grant_id><pubmed_authors>Tang Z</pubmed_authors><pubmed_authors>Hang C</pubmed_authors><pubmed_authors>Shan Z</pubmed_authors><pubmed_authors>An L</pubmed_authors><pubmed_authors>Liang Z</pubmed_authors><pubmed_authors>Cui H</pubmed_authors><pubmed_authors>Zhang L</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Shao R</pubmed_authors><pubmed_authors>Yang S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Hypothermia regulates mitophagy and apoptosis via PINK1/Parkin-VDAC 3 signaling pathway during oxygen-glucose deprivation/recovery injury.</name><description>Post-cardiac arrest brain injury (PCABI), as the main cause of high mortality and long-term disability in patients, induces mitochondrial damage and cell apoptosis. Hypothermia is well-known as an effective neuroprotective therapy, but its underlying mechanisms deserve further exploration. Previous study has demonstrated that hypothermia provides neuroprotection via increasing PINK1/Parkin-mediated mitophagy. However, whether hypothermia can regulate both apoptosis and mitophagy through the PINK1/Parkin-VDAC3 signaling pathway or not. In this study, BV2 mouse microglial cells were cultured under oxygen-glucose deprivation for 6 h following reperfusion with or without hypothermia for 2-4 h. Cell viability was examined by trypan blue stain. Mitophagy was observed by transmission electron mic</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Feb</publication><modification>2025-04-04T01:34:10.399Z</modification><creation>2025-04-04T01:34:10.399Z</creation></dates><accession>S-EPMC11806084</accession><cross_references><pubmed>39920327</pubmed><doi>10.1038/s41598-025-89176-w</doi></cross_references></HashMap>