{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["8"],"submitter":["Angebault C"],"pubmed_abstract":["Besides skeletal muscle dysfunction, Duchenne muscular dystrophy (DMD) exhibits a progressive cardiomyopathy characterized by an impaired calcium (Ca<sup>2+</sup>) homeostasis and a mitochondrial dysfunction. Here we aimed to determine whether sarco-endoplasmic reticulum (SR/ER)-mitochondria interactions and mitochondrial function were impaired in dystrophic heart at the early stage of the pathology. For this purpose, ventricular cardiomyocytes and mitochondria were isolated from 3-month-old dystrophin-deficient mice (<i>mdx</i> mice). The number of contacts points between the SR/ER Ca<sup>2+</sup> release channels (IP3R1) and the porine of the outer membrane of the mitochondria, VDAC1, measured using <i>in situ</i> proximity ligation assay, was greater in <i>mdx</i> cardiomyocytes. Expres"],"journal":["Frontiers in cell and developmental biology"],"pagination":["609493"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7868535"],"repository":["biostudies-literature"],"pubmed_title":["Metformin Reverses the Enhanced Myocardial SR/ER-Mitochondria Interaction and Impaired Complex I-Driven Respiration in Dystrophin-Deficient Mice."],"pmcid":["PMC7868535"],"pubmed_authors":["Fauconnier J","Panel M","Lacote M","Rieusset J","Lacampagne A","Angebault C"],"additional_accession":[]},"is_claimable":false,"name":"Metformin Reverses the Enhanced Myocardial SR/ER-Mitochondria Interaction and Impaired Complex I-Driven Respiration in Dystrophin-Deficient Mice.","description":"Besides skeletal muscle dysfunction, Duchenne muscular dystrophy (DMD) exhibits a progressive cardiomyopathy characterized by an impaired calcium (Ca<sup>2+</sup>) homeostasis and a mitochondrial dysfunction. Here we aimed to determine whether sarco-endoplasmic reticulum (SR/ER)-mitochondria interactions and mitochondrial function were impaired in dystrophic heart at the early stage of the pathology. For this purpose, ventricular cardiomyocytes and mitochondria were isolated from 3-month-old dystrophin-deficient mice (<i>mdx</i> mice). The number of contacts points between the SR/ER Ca<sup>2+</sup> release channels (IP3R1) and the porine of the outer membrane of the mitochondria, VDAC1, measured using <i>in situ</i> proximity ligation assay, was greater in <i>mdx</i> cardiomyocytes. Expres","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020","modification":"2025-05-29T21:49:14.513Z","creation":"2025-05-29T21:49:14.513Z"},"accession":"S-EPMC7868535","cross_references":{"pubmed":["33569379"],"doi":["10.3389/fcell.2020.609493"]}}