Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
J Cardiovasc Pharmacol. 2009 Oct;54(4):263-72. doi: 10.1097/FJC.0b013e3181ba0811.
Gap junctions (GJs) allow direct communication between cells. In the heart, GJs mediate the electrical coupling of cardiomyocytes and as such dictate the speed and direction of cardiac conduction. A prominent feature of acquired structural heart disease is remodeling of GJ protein expression and localization concomitant with increased susceptibility to lethal arrhythmias, leading many to hypothesize that the two are causally linked. Detailed understanding of the cellular mechanisms that regulate GJ localization and function within cardiomyocytes may therefore uncover potential therapeutic strategies for a significant clinical problem. This review will outline our current understanding of GJ cell biology with the intent of highlighting cellular mechanisms responsible for GJ remodeling associated with cardiac disease.
缝隙连接（GJ）允许细胞之间直接通讯。在心脏中，GJ 介导心肌细胞的电偶联，从而决定心脏传导的速度和方向。获得性结构性心脏病的一个显著特征是 GJ 蛋白表达和定位的重塑，同时增加了致命性心律失常的易感性，这使得许多人假设这两者是因果关系。因此，深入了解调节心肌细胞中 GJ 定位和功能的细胞机制，可能会为这一重大临床问题揭示潜在的治疗策略。本综述将概述我们目前对 GJ 细胞生物学的理解，旨在强调与心脏疾病相关的 GJ 重塑的细胞机制。
