Remodelling of cardiac gap junction connexin 43 and arrhythmogenesis.

Abstract

Augmentation of PKC-mediated phosphorylation and suppression of PKA-mediated phosphorylation induces the downward remodelling of Cx43. Such remodelling of Cx43 induces asynchronous electrical activities and makes the ventricular tissue susceptible to fibrillation. PKC is activated by AII. The fibrillation itself remodels Cx43, thereby causing a vicious cycle. As a result, PKC inhibitors, AII antagonists and PKA activators are considered to possibly have a protective effect against the initiation or advancement of ventricular fibrillation.