{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["15(12)"],"submitter":["Shao L"],"pubmed_abstract":["Pancreatic β-cell apoptosis plays a crucial role in the development of type 2 diabetes. Cytochrome c oxidase subunit 6A2 (COX6A2) and Farnesoid X Receptor (FXR) have been identified in pancreatic β-cells, however, whether they are involved in β-cell apoptosis is unclear. Here, we sought to investigate the role of FXR-regulated COX6A2 in diabetic β-cell apoptosis. We found that COX6A2 expression was increased in islets from diabetic animals, whereas FXR expression was suppressed. Notably, overexpression of COX6A2 facilitated β-cell apoptosis, whereas its deficiency attenuated this process and ameliorates type 2 diabetes, suggesting a pro-apoptotic role of COX6A2 in β-cells. Mechanistically, increased COX6A2 interacted with and enhanced the expression of voltage-dependent anion channel 1 (VD"],"journal":["Cell death & disease"],"pagination":["920"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11659401"],"repository":["biostudies-literature"],"pubmed_title":["FXR-regulated COX6A2 triggers mitochondrial apoptosis of pancreatic β-cell in type 2 diabetes."],"pmcid":["PMC11659401"],"pubmed_authors":["Shao L","Ma X","Ying Y","Lv S","Yan D","Shu X","Kong X","Ai X"],"additional_accession":[]},"is_claimable":false,"name":"FXR-regulated COX6A2 triggers mitochondrial apoptosis of pancreatic β-cell in type 2 diabetes.","description":"Pancreatic β-cell apoptosis plays a crucial role in the development of type 2 diabetes. Cytochrome c oxidase subunit 6A2 (COX6A2) and Farnesoid X Receptor (FXR) have been identified in pancreatic β-cells, however, whether they are involved in β-cell apoptosis is unclear. Here, we sought to investigate the role of FXR-regulated COX6A2 in diabetic β-cell apoptosis. We found that COX6A2 expression was increased in islets from diabetic animals, whereas FXR expression was suppressed. Notably, overexpression of COX6A2 facilitated β-cell apoptosis, whereas its deficiency attenuated this process and ameliorates type 2 diabetes, suggesting a pro-apoptotic role of COX6A2 in β-cells. Mechanistically, increased COX6A2 interacted with and enhanced the expression of voltage-dependent anion channel 1 (VD","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Dec","modification":"2025-04-26T17:10:37.945Z","creation":"2025-04-06T15:25:10.764Z"},"accession":"S-EPMC11659401","cross_references":{"pubmed":["39702527"],"doi":["10.1038/s41419-024-07302-4"]}}