Jennings Michelle M, Donahue J Kevin
Case Western Reserve University School of Medicine, MetroHealth Campus.
J Atr Fibrillation. 2013 Aug 31;6(2):839. doi: 10.4022/jafib.839. eCollection 2013 Aug-Sep.
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.
心房颤动通过增加中风、心力衰竭和心肌梗死的风险，显著导致死亡率和发病率上升。对心房颤动发生和维持机制的研究突出了缝隙连接重塑的重要性。连接蛋白40和43是主要的心房缝隙连接蛋白，在心房颤动时其表达和定位会发生相当大的改变，从而营造出有利于持续折返的环境。心房颤动在这种折返基质中起始和/或维持。本综述将聚焦于在心房颤动潜在机制及可能治疗靶点背景下的连接蛋白重塑。
