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Gap junction remodelling in human heart failure is associated with increased interaction of connexin43 with ZO-1

机译:人类心力衰竭中的间隙连接重塑与连接蛋白43与ZO-1相互作用的增加有关

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摘要

Aims Remodelling of gap junctions, involving reduction of total gap junction quantity and down-regulation of connexin43 (Cx43), contributes to the arrhythmic substrate in congestive heart failure. However, little is known of the underlying mechanisms. Recent studies from in vitro systems suggest that the connexin-interacting protein zonula occludens-1 (ZO-1) is a potential mediator of gap junction remodelling. We therefore examined the hypothesis that ZO-1 contributes to reduced expression of Cx43 gap junctions in congestive heart failure.
机译:目的间隙连接的重塑,包括减少总间隙连接数量和下调连接蛋白43(Cx43),有助于充血性心力衰竭的心律失常。但是,对底层机制知之甚少。体外系统的最新研究表明,与连接蛋白相互作用的小带闭合蛋白1(ZO-1)是间隙连接重塑的潜在介体。因此,我们检查了ZO-1有助于充血性心力衰竭的Cx43间隙连接减少表达的假说。

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