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Selective Connexin43 Inhibition Prevents Isoproterenol-Induced Arrhythmias and Lethality in Muscular Dystrophy Mice
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Selective Connexin43 Inhibition Prevents Isoproterenol-Induced Arrhythmias and Lethality in Muscular Dystrophy Mice
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Journal Article
Selective Connexin43 Inhibition Prevents Isoproterenol-Induced Arrhythmias and Lethality in Muscular Dystrophy Mice
2015
Overview
Duchenne muscular dystrophy (DMD) is caused by an X-linked mutation that leads to the absence of dystrophin, resulting in life-threatening arrhythmogenesis and associated heart failure. We targeted the gap junction protein connexin43 (Cx43) responsible for maintaining cardiac conduction. In mild
mdx
and severe
mdx:utr
mouse models of DMD and human DMD tissues, Cx43 was found to be pathologically mislocalized to lateral sides of cardiomyocytes. In addition, overall Cx43 protein levels were markedly increased in mouse and human DMD heart tissues examined. Electrocardiography on isoproterenol challenged mice showed that both models developed arrhythmias and died within 24 hours, while wild-type mice were free of pathology. Administering peptide mimetics to inhibit lateralized Cx43 function prior to challenge protected
mdx
mice from arrhythmogenesis and death, while
mdx:utr
mice displayed markedly improved ECG scores. These findings suggest that Cx43 lateralization contributes significantly to DMD arrhythmogenesis and that selective inhibition may provide substantial benefit.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Animals
/ Arrhythmias, Cardiac - drug therapy
/ Arrhythmias, Cardiac - pathology
/ Connexin 43 - antagonists & inhibitors
/ Duchenne's muscular dystrophy
/ EKG
/ Female
/ Humanities and Social Sciences
/ Humans
/ Male
/ Mice
/ Muscular Dystrophy, Animal - complications
/ Muscular Dystrophy, Animal - pathology
/ Muscular Dystrophy, Duchenne - complications
/ Muscular Dystrophy, Duchenne - pathology
/ Rodents
/ Science
