{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["15(1)"],"submitter":["Tsui KH"],"pubmed_abstract":["The female reproductive system is quite sensitive to regulation, and external environmental stimuli may cause oxidative stress which in turn may lead to accelerated aging and programmed cell death in female reproductive cells. The aim of this study was to investigate whether or not mitoquinone (MitoQ) could resist ROS-induced apoptosis in human granulosa cells and mouse oocytes. We found that the MitoQ treatment significantly reduced production of reactive oxygen species (ROS) and imbalance in mitochondrial membrane potential. The MitoQ treatment prevented an excessive mitochondrial fragmentation by upregulating Drp1 S637 and decreasing Drp1 S637 phosphorylation. More importantly, MitoQ maintained aerobic respiration and reduced anaerobic respiration by regulating reprogramming of intracel"],"journal":["Aging"],"pagination":["246-260"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9876626"],"repository":["biostudies-literature"],"pubmed_title":["Mitoquinone shifts energy metabolism to reduce ROS-induced oxeiptosis in female granulosa cells and mouse oocytes."],"pmcid":["PMC9876626"],"pubmed_authors":["Tsui KH","Li CJ"],"additional_accession":[]},"is_claimable":false,"name":"Mitoquinone shifts energy metabolism to reduce ROS-induced oxeiptosis in female granulosa cells and mouse oocytes.","description":"The female reproductive system is quite sensitive to regulation, and external environmental stimuli may cause oxidative stress which in turn may lead to accelerated aging and programmed cell death in female reproductive cells. The aim of this study was to investigate whether or not mitoquinone (MitoQ) could resist ROS-induced apoptosis in human granulosa cells and mouse oocytes. We found that the MitoQ treatment significantly reduced production of reactive oxygen species (ROS) and imbalance in mitochondrial membrane potential. The MitoQ treatment prevented an excessive mitochondrial fragmentation by upregulating Drp1 S637 and decreasing Drp1 S637 phosphorylation. More importantly, MitoQ maintained aerobic respiration and reduced anaerobic respiration by regulating reprogramming of intracel","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2025-04-22T06:31:33.306Z","creation":"2025-04-05T21:47:07.325Z"},"accession":"S-EPMC9876626","cross_references":{"pubmed":["36626243"],"doi":["10.18632/aging.204475"]}}