Downregulation and reduced phosphorylation of Cx43, along with increased fibrosis, contribute to the arrhythmogenic substrate in end-stage nonischemic cardiomyopathy.
Conduction disorder resulting from the anisotropic downregulation of Cx43 expression, the reduction of Cx43 phosphorylation, and increased fibrosis is likely to be a critical component of arrhythmogenic substrate in patients with nonischemic cardiomyopathy.
Glukhov et al. (Tue,) studied this question.
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