ArticleCardiovascular research2026
Reduced Cx43 S-nitrosylation protects against cardiac stress-induced arrhythmias and myocardial injury in Duchenne muscular dystrophy.
Article in Cardiovascular research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
aimsIn Duchenne muscular dystrophy (DMD), connexin-43 (Cx43) delocalizes from intercalated discs to the lateral membrane of cardiomyocytes, where it forms undocked hemichannels. β-adrenergic stress induces lethal arrhythmias in DMDmdx mice that correlate with increased Cx43 S-nitrosylation and excessive hemichannel opening. Here, we aimed to determine whether S-nitrosylation of Cx43 at cysteine 271 directly contributes to β-adrenergic stress-induced arrhythmias and myocardial injury in DMD. METHODS AND
resultsTo define the role of Cx43 S-nitrosylation in DMD cardiomyopathy, we generated DMDmdx knock-in mice carrying a cysteine-to-serine substitution at residue 271, a critical S-nitrosylation site involved in NO-dependent Cx43 hemichannel activation (DMDmdx:C271S+/-). Following β-adrenergic stimulation, DMDmdx mice exhibited a higher incidence of arrhythmogenic events and increased triggered activity in isolated cardiomyocytes compared with DMDmdx:C271S+/- mice, which more closely resembled wild-type mice. Optical mapping of isolated hearts showed that DMDmdx mice developed abnormal Ca2+ transients, prolonged action potentials, and episodes of conduction block. These abnormalities were normalized in DMDmdx:C271S+/- mice and attenuated by treatment with the Cx43 hemichannel inhibitor Gap19. Moreover, β-adrenergic stress evoked severe myocardial injury and bradycardia in DMDmdx mice, both of which were significantly attenuated in DMDmdx:C271S+/- mice. Notably, Gap19-treated DMDmdx mice were protected against myocardial injury, further supporting a direct role for Cx43 hemichannels in DMD-associated cardiac damage.
conclusionThese findings reveal, for the first time, a mechanistic link between Cx43 hemichannel activity, arrhythmogenesis, and myocardial injury in DMD. We conclude that S-nitrosylation of Cx43 is a fundamental NO-mediated mechanism driving β-adrenergic stress-induced arrhythmias and myocardial injury in DMDmdx mice through pathological opening of Cx43 hemichannels.
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