{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["He J"],"funding":["NIDDK NIH HHS","Fondation Leducq","NHLBI NIH HHS","National Institutes of Health"],"pagination":["97"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4526192"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14"],"pubmed_abstract":["<h4>Background</h4>In diabetes mellitus the morbidity and mortality of cardiovascular disease is increased and represents an important independent mechanism by which heart disease is exacerbated. The pathogenesis of diabetic cardiomyopathy involves the enhanced activation of PPAR transcription factors, including PPARα, and to a lesser degree PPARβ and PPARγ1. How these transcription factors are regulated in the heart is largely unknown. Recent studies have described post-translational ubiquitination of PPARs as ways in which PPAR activity is inhibited in cancer. However, specific mechanisms in the heart have not previously been described. Recent studies have implicated the muscle-specific ubiquitin ligase muscle ring finger-2 (MuRF2) in inhibiting the nuclear transcription factor SRF. Init"],"journal":["Cardiovascular diabetology"],"pubmed_title":["MuRF2 regulates PPARγ1 activity to protect against diabetic cardiomyopathy and enhance weight gain induced by a high fat diet."],"pmcid":["PMC4526192"],"funding_grant_id":["P30 DK056350","R01HL104129","DK056350","R01 HL104129","Transatlantic Network of Excellence"],"pubmed_authors":["L Parry T","Mapanga RF","He J","J Grevengoed T","Hill JA","Sullivan J","Han Y","Quintana MT","Willis MS","Schisler JC","Stansfield WE","Clarke BA","Muehlbauer MJ","Essop MF","Newgard CB","Yates CC","Bain JR"],"additional_accession":[]},"is_claimable":false,"name":"MuRF2 regulates PPARγ1 activity to protect against diabetic cardiomyopathy and enhance weight gain induced by a high fat diet.","description":"<h4>Background</h4>In diabetes mellitus the morbidity and mortality of cardiovascular disease is increased and represents an important independent mechanism by which heart disease is exacerbated. The pathogenesis of diabetic cardiomyopathy involves the enhanced activation of PPAR transcription factors, including PPARα, and to a lesser degree PPARβ and PPARγ1. How these transcription factors are regulated in the heart is largely unknown. Recent studies have described post-translational ubiquitination of PPARs as ways in which PPAR activity is inhibited in cancer. However, specific mechanisms in the heart have not previously been described. Recent studies have implicated the muscle-specific ubiquitin ligase muscle ring finger-2 (MuRF2) in inhibiting the nuclear transcription factor SRF. Init","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Aug","modification":"2026-05-30T10:54:07.782Z","creation":"2019-03-26T22:33:02Z"},"accession":"S-EPMC4526192","cross_references":{"pubmed":["26242235"],"doi":["10.1186/s12933-015-0252-x"]}}