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首页> 外文期刊>Biochimica et biophysica acta. Biomembranes >Mitochondrial Cx43, an important component of cardiac preconditioning
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Mitochondrial Cx43, an important component of cardiac preconditioning

机译：线粒体CX43，心脏预处理的重要组成部分

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Abstract Connexin 43 (Cx43) forms gap junction channels that are essential for the propagation of electrical depolarization in cardiomyocytes, but also with important roles in the pathophysiology of reperfusion injury. However, more recent studies have shown that Cx43 has also important functions independent from intercellular communication between adjacent cardiomyocytes. Some of these actions have been related to the presence of Cx43 in the mitochondria of these cells (mitoCx43). The functions of mitoCx43 have not been completely elucidated, but there is strong evidence indicating that mitoCx43 modulates mitochondrial respiration at respiratory complex I, production of radical oxygen species and ATP synthesis. These functions of mitoCx43 modulate mitochondrial and cellular tolerance to reperfusion after prolonged ischemia and are necessary for the cardioprotective effect of ischemic preconditioning. In the present review article we discuss available knowledge on these functions of mitoCx43 in relation to reperfusion injury, the molecular mechanisms involved and explore the possibility that mitoCx43 may constitute a new pharmacological target in patients with ST-segment elevation myocardial infarction (STEMI). This article is part of a Special Issue entitled: Gap Junction Proteins edited by Jean Claude Herve. Graphical abstract Display Omitted Highlights ? Connexin 43 (Cx43) is present at the inner mitochondrial membrane of subsarcolemmal cardiomyocyte mitochondria (mitoCx43). ? MitoCx43 modulates mitochondrial respiration and ATP synthesis, and production of radical oxygen species. ? MitoCx43 modulates reperfusion injury and decreases the tolerance of ischemic cardiomyocytes to reperfusion. ? MitoCx43 is necessary for the cardioprotective effect of ischemic preconditioning.
机译：摘要Connexin 43（CX43）形成用于在心肌细胞中繁殖的电解化繁殖的间隙结沟，但也具有在再灌注损伤的病理生理学中的重要作用。然而，最近的研究表明，CX43也具有独立于相邻心肌细胞之间的细胞间通信的重要功能。其中一些动作与这些细胞的线粒体中CX43的存在有关（Mitocx43）。 Mitocx43的功能尚未完全阐明，但存在强有力的证据表明Mitocx43在呼吸络合物I中调节线粒体呼吸，产生自由基氧物质和ATP合成。 Mitocx43的这些功能调节线粒体和细胞耐受，在延长缺血后再灌注，并且是缺血预处理的心脏保护作用所必需的。在本综述文章中，我们讨论了对重新灌注损伤的Mitocx43的这些功能的可用知识，所涉及的分子机制和探讨Mitocx43可能构成ST段升高心肌梗死（STEMI）的新药理学靶标的可能性。本文是题为的特殊问题的一部分：Jean Claude Herve编辑的Gap Junction蛋白。图形抽象显示省略了亮点？ Connexin 43（CX43）存在于子思索心肌细胞线粒体（Mitocx43）的内部线粒体膜处。还Mitocx43调节线粒体呼吸和ATP合成，并产生自由基氧。还Mitocx43调节再灌注损伤并降低缺血性心肌细胞的耐受再灌注。还Mitocx43对于缺血预处理的心脏保护作用是必要的。

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