Functional consequences of abnormal Cx43 expression in the heart
Functional consequences of abnormal Cx43 expression in the heart
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DOI：
10.1016/j.bbamem.2011.07.039
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发表时间：
2012-08-01
影响因子：
3.4
通讯作者：
van Rijen, Harold V. M.
中科院分区：
文献类型：
--
作者：
Fontes, Magda S. C.;van Veen, Loon A. B.;van Rijen, Harold V. M.
在心脏中表达的主要间隙连接蛋白，连接蛋白43（Cx43），在患病的心脏中高度重构。通常，Cx43下调并不均匀地重新分布到心肌细胞的侧面。Cx43表达受损的逆转重构可以恢复正常的心脏功能和正常的电稳定性。在这篇综述中，减少和异质性Cx43在心脏中的表达将被解决在肥厚性，扩张性和缺血性心肌病连同其功能的传导速度减慢，分散的冲动传导，其相互作用与纤维化和倾向于产生心律失常的后果。最后，讨论了不同的治疗方法。旨在改善Cx43表达水平的治疗显示了心力衰竭期间新的潜在抗心肌梗死疗法，但在急性缺血的背景下，这些治疗可能是以较大梗死面积为代价的抗心肌梗死疗法。本文是特刊的一部分，题为：沟通的枢纽，组成，结构和特点。(C)2011 Elsevier B.V.保留所有权利。
The major gap junction protein expressed in the heart, connexin43 (Cx43), is highly remodeled in the diseased heart. Usually, Cx43 is down-regulated and heterogeneously redistributed to the lateral sides of cardiomyocytes. Reverse remodeling of the impaired Cx43 expression could restore normal cardiac function and normalize electrical stability. In this review, the reduced and heterogeneous Cx43 expression in the heart will be addressed in hypertrophic, dilated and ischemic cardiomyopathy together with its functional consequences of conduction velocity slowing, dispersed impulse conduction, its interaction with fibrosis and propensity to generate arrhythmias. Finally, different therapies are discussed. Treatments aimed to improve the Cx43 expression levels show new potentially anti-arrhythmic therapies during heart failure, but those in the context of acute ischemia can be anti-arrhythmogenic at the cost of larger infarct sizes. This article is part of a Special Issue entitled: The Communicating junctions, composition, structure and characteristics. (C) 2011 Elsevier B.V. All rights reserved.