carbon monoxide improves cardiac function and mitochondrial population quality in a mouse model of metabolic syndrome一氧化碳可以改善心脏功能和线粒体代谢综合征小鼠模型的人口素质.pdfVIP

Carbon Monoxide Improves Cardiac Function and Mitochondrial Population Quality in a Mouse Model of Metabolic Syndrome 1 1 1 1 1 Steve Lancel *, David Montaigne , Xavier Marechal , Camille Marciniak , Sidi Mohamed Hassoun , 1 1 1 2 3 Brigitte Decoster , Caroline Ballot , Caroline Blazejewski , Delphine Corseaux , Bernadette Lescure , Roberto Motterlini4, Remi Neviere1 1 EA4484, Physiology Department, Lille 2 University, Lille, France, 2 EA2693, Lille 2 University, Lille, France, 3 INSERM IFR65, Institut de Recherche en Sante Saint Antoine ´ (Irssa), Faculty of Medicine, Paris, France, 4 INSERM U955, Faculty of Medicine, Paris-Est University, Creteil, France Abstract Aims: Metabolic syndrome induces cardiac dysfunction associated with mitochondria abnormalities. As low levels of carbon monoxide (CO) may improve myocardial and mitochondrial activities, we tested whether a CO-releasing molecule (CORM-3) reverses metabolic syndrome-induced cardiac alteration through changes in mitochondrial biogenesis, dynamics and autophagy. Methods and Results: Mice were fed with normal diet (ND) or high-fat diet (HFD) for twelve weeks. Then, mice received two intraperitoneal injections of CORM-3 (10 mg.kg21), with the second one given 16 hours after the first. Contractile function in isolated hearts and mitochondrial parameters were evaluated 24 hours after the last injection. Mitochondrial population was explored by electron microscopy. Changes in mitochondrial