Abstract

Connexin 43 (Cx43) is the most abundant connexin forming gap junction channels in heart. In multiple cardiac pathologies, Cx43 is found remodeled at the lateralize side of unhealthy cardiomyocytes. We recently demonstrated that remodeled Cx43 protein functions as non-junctional channels (hemichannels) in a Duchene muscular dystrophy (DMD) mouse model. These mice were susceptible to arrhythmias upon β-adrenergic stress; however, arrhythmias were prevented using Cx43 hemichannel blockers and by genetically reducing Cx43 levels.

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