biostudies-literatureUnknown8Angebault CBesides skeletal muscle dysfunction, Duchenne muscular dystrophy (DMD) exhibits a progressive cardiomyopathy characterized by an impaired calcium (Ca²⁺) 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 Ca²⁺ 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. ExpresFrontiers in cell and developmental biology609493https://www.ebi.ac.uk/biostudies/studies/S-EPMC7868535biostudies-literatureMetformin Reverses the Enhanced Myocardial SR/ER-Mitochondria Interaction and Impaired Complex I-Driven Respiration in Dystrophin-Deficient Mice.PMC7868535Fauconnier JPanel MLacote MRieusset JLacampagne AAngebault CfalseMetformin Reverses the Enhanced Myocardial SR/ER-Mitochondria Interaction and Impaired Complex I-Driven Respiration in Dystrophin-Deficient Mice.Besides skeletal muscle dysfunction, Duchenne muscular dystrophy (DMD) exhibits a progressive cardiomyopathy characterized by an impaired calcium (Ca²⁺) 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 Ca²⁺ 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. Expres2020-01-01T00:00:00Z20202025-05-29T21:49:14.513Z2025-05-29T21:49:14.513ZS-EPMC78685353356937910.3389/fcell.2020.609493