{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Da Dalt L"],"funding":["Ministero dell&amp;apos;Istruzione dell&amp;apos;Università e della Ricerca","Vetenskapsrådet","Fondazione Umberto Veronesi","Skånes universitetssjukhus","Region Skåne","Knut och Alice Wallenbergs Stiftelse","Ettevõtluse Arendamise Sihtasutus","STROKE-Riksförbundet","European Atherosclerosis Society","Lund University Medical Faculty Foundation","Svenska Sällskapet för Medicinsk Forskning","Stiftelsen för Strategisk Forskning","Hjärt-Lungfonden","Lunds Universitet"],"pagination":["102256"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12538947"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["102"],"pubmed_abstract":["<h4>Objective</h4>Mitochondria are involved in cellular metabolism, energy production, calcium homeostasis, and the synthesis of sterols and bile acids (BAs). Emerging evidence suggests that mitochondrial dynamics including biogenesis, fusion, fission, and mitophagy critically influence cardiometabolic diseases, yet their role in atherogenesis remain poorly understood. Mitochondrial fusion ensures metabolic flexibility and stress adaptation, processes highly relevant to lipid handling and vascular cell plasticity. OPA1, a key regulator of inner mitochondrial membrane fusion, has been implicated in metabolic remodeling and cellular stress responses. We therefore investigated whether modulation of OPA1 expression affects lipid homeostasis and plaque formation in LDL receptor-deficient (LDLR "],"journal":["Molecular metabolism"],"pubmed_title":["Increased mitochondrial fusion via systemic OPA1 overexpression promotes dyslipidemia and atherosclerosis in LDLR deficient mice."],"pmcid":["PMC12538947"],"funding_grant_id":["CG-22-0254-H-02","S-993166","2023","20241210","2019-01260","2023\\u201302368","IRC15-0067","20200403","20220044","22CVD02","20220284","2019-01907","2009-1039","20230257","2024\\u201302761"],"pubmed_authors":["Giancane G","Moregola A","Donetti E","Mitro N","Fantini F","Scorrano L","Da Dalt L","Edsfeldt A","Uboldi P","Goncalves I","Roda S","Baragetti A","Norata GD","Vingiani GB","Pedretti S","Svecla M","Sun J"],"additional_accession":[]},"is_claimable":false,"name":"Increased mitochondrial fusion via systemic OPA1 overexpression promotes dyslipidemia and atherosclerosis in LDLR deficient mice.","description":"<h4>Objective</h4>Mitochondria are involved in cellular metabolism, energy production, calcium homeostasis, and the synthesis of sterols and bile acids (BAs). Emerging evidence suggests that mitochondrial dynamics including biogenesis, fusion, fission, and mitophagy critically influence cardiometabolic diseases, yet their role in atherogenesis remain poorly understood. Mitochondrial fusion ensures metabolic flexibility and stress adaptation, processes highly relevant to lipid handling and vascular cell plasticity. OPA1, a key regulator of inner mitochondrial membrane fusion, has been implicated in metabolic remodeling and cellular stress responses. We therefore investigated whether modulation of OPA1 expression affects lipid homeostasis and plaque formation in LDL receptor-deficient (LDLR ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-06-04T15:12:20.246Z","creation":"2026-05-10T03:11:37.336Z"},"accession":"S-EPMC12538947","cross_references":{"pubmed":["40992730"],"doi":["10.1016/j.molmet.2025.102256"]}}