{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang L"],"funding":["Beijing Hospitals Authority's Ascent Plan","High-Level Public Health Technical Talent Building Program","National Natural Science Foundation of China","Capital's Funds for Health Improvement and Research"],"pagination":["4607"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11806084"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"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"],"journal":["Scientific reports"],"pubmed_title":["Hypothermia regulates mitophagy and apoptosis via PINK1/Parkin-VDAC 3 signaling pathway during oxygen-glucose deprivation/recovery injury."],"pmcid":["PMC11806084"],"funding_grant_id":["82072136","CFH 2022-1-2032","Discipline Leader-01-01","DFL20240302"],"pubmed_authors":["Tang Z","Hang C","Shan Z","An L","Liang Z","Cui H","Zhang L","Wang X","Shao R","Yang S"],"additional_accession":[]},"is_claimable":false,"name":"Hypothermia regulates mitophagy and apoptosis via PINK1/Parkin-VDAC 3 signaling pathway during oxygen-glucose deprivation/recovery injury.","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","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Feb","modification":"2025-04-04T01:34:10.399Z","creation":"2025-04-04T01:34:10.399Z"},"accession":"S-EPMC11806084","cross_references":{"pubmed":["39920327"],"doi":["10.1038/s41598-025-89176-w"]}}