The Na+/Ca²+ exchanger in cardiac ischemia/reperfusion injury.
The Na+/Ca²+ exchanger in cardiac ischemia/reperfusion injury.
复制标题
Na/Ca2交换体在心脏缺血/再灌注损伤中的作用
DOI：
10.12659/msm.883533
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发表时间：
2012-11
期刊：
影响因子：
--
通讯作者：
Li S
中科院分区：
文献类型：
--
作者：
Chen S;Li S
Na+/Ca2+交换器（NCX）是哺乳动物多种器官中维持Na+和Ca2+稳态的重要电致转运体，并参与心肌中Ca2+浓度的生理和病理生理调节。它可以影响心脏结构、电生理和收缩特性。NCX在缺血/再灌注（IR）后心脏细胞中的作用已经通过许多体外和体内模型进行了研究。在缺血期间，离子干扰有利于Ca2+内流模式活动，因为过量的Na+被挤出以换取Ca2+，导致细胞内Ca2+水平增加（Cai）。这种升高导致再灌注时可逆性细胞功能障碍，如心肌坏死、心律失常、收缩功能障碍和心力衰竭。我们回顾了主要的体内和体外心脏IR相关的NCX研究，试图阐明NCX在IR中的功能，并得出结论，最近的研究表明NCX阻断具有潜在的治疗应用。尽管不同IR模型的使用、NCX刺激剂和抑制剂的应用以及NCX转基因动物的开发有助于阐明这种离子交换剂在心脏细胞中的作用，但相关机制尚不完全清楚，临床有效的特异性NCX抑制剂有待进一步研究。
Summary The Na+/Ca2+ exchanger (NCX) is an important electrogenic transporter in maintaining Na+ and Ca2+ homeostasis in a variety of mammalian organs, and is involved in the physiological and pathophysiological regulation of Ca2+ concentration in the myocardium. It can affect cardial structure, electrophysiology and contractile properties. The role of the NCX in heart cells following ischemia/reperfusion (IR) has been investigated using a number of in vitro and in vivo models. During ischemia, ionic disturbances favor Ca2+-influx mode activity as excess Na+ is extruded in exchange for Ca2+, giving rise to increased intracellular Ca2+ levels (Cai). This rise in Cai contributes to reversible cellular dysfunction upon reperfusion, such as myocardial necrosis, arrhythmia, systolic dysfunction and heart failure. We have reviewed the major in vivo and in vitro cardiac IR-related NCX studies in an attempt to clarify the functions of NCX in IR and conclude that recent studies suggest blockage of NCX has potential therapeutic applications. Although the use of different IR models, application of NCX stimulators and inhibitors, and development of NCX transgenic animals do help elucidate the role of this ion exchanger in heart cells, related mechanisms are not completely understood and clinically effective specific NCX inhibitors need further research.
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