{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chang CF"],"funding":["NIDDK NIH HHS","NIH HHS","NIGMS NIH HHS"],"pagination":["14"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9854525"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(1)"],"pubmed_abstract":["Coenzyme Q (CoQ, aka ubiquinone) is a key component of the mitochondrial electron transport chain (ETC) and membrane-incorporated antioxidant. CoQ10 deficiencies encompass a heterogeneous spectrum of clinical phenotypes and can be caused by hereditary mutations in the biosynthesis pathway or result from pharmacological interventions such as HMG-CoA Reductase inhibitors, and statins, which are widely used to treat hypercholesterolemia and prevent cardiovascular disease. How CoQ deficiency affects individual tissues and cell types, particularly mitochondrial-rich ones such as brown adipose tissue (BAT), has remained poorly understood. Here we show that pharmacological and genetic models of BAT CoQ deficiency show altered respiration that can only in part be explained by classical roles of Co"],"journal":["Antioxidants (Basel, Switzerland)"],"pubmed_title":["CoQ Regulates Brown Adipose Tissue Respiration and Uncoupling Protein 1 Expression."],"pmcid":["PMC9854525"],"funding_grant_id":["R01DK126830","R01DK118727","R01DK089202","R01 DK089202","R35 GM136415","R01 DK126830"],"pubmed_authors":["Chang CF","Gunawan AL","Zushin PH","Liparulo I","Bertholet AM","Kirichok Y","Stahl A"],"additional_accession":[]},"is_claimable":false,"name":"CoQ Regulates Brown Adipose Tissue Respiration and Uncoupling Protein 1 Expression.","description":"Coenzyme Q (CoQ, aka ubiquinone) is a key component of the mitochondrial electron transport chain (ETC) and membrane-incorporated antioxidant. CoQ10 deficiencies encompass a heterogeneous spectrum of clinical phenotypes and can be caused by hereditary mutations in the biosynthesis pathway or result from pharmacological interventions such as HMG-CoA Reductase inhibitors, and statins, which are widely used to treat hypercholesterolemia and prevent cardiovascular disease. How CoQ deficiency affects individual tissues and cell types, particularly mitochondrial-rich ones such as brown adipose tissue (BAT), has remained poorly understood. Here we show that pharmacological and genetic models of BAT CoQ deficiency show altered respiration that can only in part be explained by classical roles of Co","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Dec","modification":"2025-04-04T10:19:49.417Z","creation":"2025-02-19T00:12:28.897Z"},"accession":"S-EPMC9854525","cross_references":{"pubmed":["36670876"],"doi":["10.3390/antiox12010014"]}}