连接蛋白43与缺血预处理。

Rainer Schulz, Gerd Heusch
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引用次数: 40

摘要

Connexin43 (Cx43)是心肌中形成半通道和间隙连接的必需蛋白。受多种蛋白激酶和磷酸酶调控的Cx43的磷酸化状态决定了半通道和/或间隙连接的电导率和通透性。间隙连接参与细胞-细胞偶联,而半通道参与心肌细胞体积调节。cx43形成的通道与缺血/再灌注损伤有关,因为阻断大部分cx43形成的通道可减轻缺血过度挛缩、梗死发展和心肌梗死后重构。缺血预处理的保护作用还依赖于功能性Cx43形成的通道,因为通道解偶联或遗传性Cx43缺乏会消除缺血预处理对梗死面积的减少。Cx43如何介导保护的确切潜在机制仍有待确定。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Connexin43 and ischemic preconditioning.

Connexin43 (Cx43) is the essential protein to form hemichannels and gap junctions in the myocardium. The phosphorylation status of Cx43 which is regulated by a variety of protein kinases and phosphatases determines hemichannel and/or gap junction conductance and permeability. Gap junctions are involved in cell-cell coupling while hemichannels contribute to cardiomyocyte volume regulation. Cx43-formed channels are involved in ischemia/reperfusion injury, since blockade of a large portion of Cx43-formed channels attenuates ischemic hypercontracture, infarct development and post myocardial infarction remodeling. Ischemic preconditioning's protection also depends on functional Cx43-formed channels, since uncoupling of channels or genetic Cx43 deficiency abolishes infarct size reduction by ischemic preconditioning. The exact underlying mechanism(s) how Cx43 mediates protection remain to be established.

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