Schulz Rainer, Heusch Gerd
Institut für Pathophysiologie, Zentrum für Innere Medizin, Universitätsklinikum Essen, Essen, Germany.
Adv Cardiol. 2006;42:213-227. doi: 10.1159/000092571.
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.
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。