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连接蛋白43与缺血预处理

Connexin43 and ischemic preconditioning.

作者信息

Schulz Rainer, Heusch Gerd

机构信息

Institut für Pathophysiologie, Zentrum für Innere Medizin, Universitätsklinikum Essen, Essen, Germany.

出版信息

Adv Cardiol. 2006;42:213-227. doi: 10.1159/000092571.

Abstract

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.

摘要

连接蛋白43(Cx43)是心肌中形成半通道和缝隙连接的必需蛋白质。Cx43的磷酸化状态受多种蛋白激酶和磷酸酶调控,决定了半通道和/或缝隙连接的电导和通透性。缝隙连接参与细胞间偶联,而半通道有助于心肌细胞容积调节。Cx43形成的通道参与缺血/再灌注损伤,因为阻断大部分Cx43形成的通道可减轻缺血性高收缩、梗死发展及心肌梗死后重塑。缺血预处理的保护作用也依赖于功能性Cx43形成的通道,因为通道解偶联或Cx43基因缺陷会消除缺血预处理对梗死面积的缩小作用。Cx43介导保护作用的确切潜在机制仍有待确定。

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