Abstract
Atrial fibrillation significantly contributes to mortality and morbidity through increased risk of stroke, heart failure and myocardial infarction. Investigations of mechanisms responsible for the development and maintenance of atrial fibrillation have highlighted the importance of gap junctional remodeling. Connexins 40 and 43, the major atrial gap junctional proteins, undergo considerable alterations in expression and localization in atrial fibrillation, creating an environment conducive to sustained reentry. Atrial fibrillation is initiated and/or maintained in this reentrant substrate. This review will focus on connexin remodeling in the context of underlying mechanism and possible therapeutic target for atrial fibrillation.
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