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缝隙连接蛋白43与心肌缺血/再灌注损伤机制的研究进展

Progress in gap junctional connexin 43 and myocardial ischemia/reperfusion injury
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摘要 背景研究表明,心肌缺血/再灌注(ischemia/reperfusion,I/R)损伤的发病机制与氧自由基过量产生、钙超载、线粒体损伤及心肌细胞凋亡等密切相关,最新研究发现缝隙连接(gapjunction,GJ)也参与心肌I/R损伤。目的现主要针对GJ连接蛋白(connexin,Cx)43与心肌I/R损伤的关系作一综述。内容Cx43在心肌I/R损伤中参与心肌保护作用,其机制可能与钙超载、在线粒体中的分布及细胞凋亡等因素相关。趋向未来研究需要进一步探究Cx43与心肌细胞凋亡之间的关系,同时为临床实际工作提供依据。 Background The mechanism of myocardial ischemia/reperfusion (I/R) involves in peroxidation, calcium overload, mitochondria injury, myocardial cells apoptosis and so on. Recent sdudies indicate that the gap junctional(GJ) intercellular communication of myocardial cells may play a role in myocardial I/R injury. Objective This article summarized the relationship between the GJ connexin (Cx) 43 and myocardial I/R injury. Content Cx43 could protected myocardium from I/R injury. The mechanism may be related with calcium overload, mitochondria injury, myocardial cells apoptosis and so on. Trend Researches in future should be taken to further explore of the relation between Cx43 and apoptosis, and strengthen the cilinial applications.
作者 韩霜 容俊芳
出处 《国际麻醉学与复苏杂志》 CAS 2013年第12期1139-1141,共3页 International Journal of Anesthesiology and Resuscitation
关键词 连接蛋白43 缝隙接合部 心肌再灌注损伤 Connexin 43 Gap Junctions Myocardial reperfusion injury
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参考文献21

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