{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ljubojevic-Holzer S"],"funding":["BioTechMed-Graz [Young Researcher Groups","Austrian Science Fund FWF","Medical University of Graz scholarship","European Society of Cardiology and Austrian Society of Cardiology"],"pagination":["1492-1505"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9074988"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["118(6)"],"pubmed_abstract":["<h4>Aims</h4>Autophagy protects against the development of cardiac hypertrophy and failure. While aberrant Ca2+ handling promotes myocardial remodelling and contributes to contractile dysfunction, the role of autophagy in maintaining Ca2+ homeostasis remains elusive. Here, we examined whether Atg5 deficiency-mediated autophagy promotes early changes in subcellular Ca2+ handling in ventricular cardiomyocytes, and whether those alterations associate with compromised cardiac reserve capacity, which commonly precedes the onset of heart failure.<h4>Methods and results</h4>RT-qPCR and immunoblotting demonstrated reduced Atg5 gene and protein expression and decreased abundancy of autophagy markers in hypertrophied and failing human hearts. The function of ATG5 was examined using cardiomyocyte-spe"],"journal":["Cardiovascular research"],"pubmed_title":["Loss of autophagy protein ATG5 impairs cardiac capacity in mice and humans through diminishing mitochondrial abundance and disrupting Ca2+ cycling."],"pmcid":["PMC9074988"],"funding_grant_id":["V 530","P27637-B28","I3301-MINOTAUR"],"pubmed_authors":["Kling KM","von Lewinski D","Sedej S","Nickel A","Kohlhaas M","Ljubojevic-Holzer S","Herbst V","Abdellatif M","Zirlik A","Muhlfeld C","Schmidt M","Maack C","Kraler S","Djalinac N","Schipke J","Scherr D","Voglhuber J","Franke GT","Rainer PP"],"additional_accession":[]},"is_claimable":false,"name":"Loss of autophagy protein ATG5 impairs cardiac capacity in mice and humans through diminishing mitochondrial abundance and disrupting Ca2+ cycling.","description":"<h4>Aims</h4>Autophagy protects against the development of cardiac hypertrophy and failure. While aberrant Ca2+ handling promotes myocardial remodelling and contributes to contractile dysfunction, the role of autophagy in maintaining Ca2+ homeostasis remains elusive. Here, we examined whether Atg5 deficiency-mediated autophagy promotes early changes in subcellular Ca2+ handling in ventricular cardiomyocytes, and whether those alterations associate with compromised cardiac reserve capacity, which commonly precedes the onset of heart failure.<h4>Methods and results</h4>RT-qPCR and immunoblotting demonstrated reduced Atg5 gene and protein expression and decreased abundancy of autophagy markers in hypertrophied and failing human hearts. The function of ATG5 was examined using cardiomyocyte-spe","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 May","modification":"2025-04-03T22:22:26.094Z","creation":"2024-12-03T23:39:17.808Z"},"accession":"S-EPMC9074988","cross_references":{"pubmed":["33752242"],"doi":["10.1093/cvr/cvab112"]}}