钠钙交换体与肾缺血再灌注损伤

钠钙交换体（sodium calcium exchanger,NCX）是一种广泛分布于膜性结构（细胞质膜、线粒体膜和分泌小泡膜等）上的阳离子转运蛋白，具有前向模式和反向模式。通过这种双向模式，可以对胞质内的Ca2+浓度进行快速精准的调节，继而影响细胞的一系列生理活动。而肾缺血再灌注时，NCX反向模式的异常激活可介导细胞Ca2+超载，进而触发一系列有害代谢反应导致细胞损伤和死亡。目前，选择性抑制NCX反向模式的苯氧基衍生物得到了较多研究，并成为治疗肾缺血再灌注损伤的新药物靶点。

Sodium calcium exchanger and renal ischemia reperfusion injury

Sodium calcium exchanger (NCX), which is widely expressed in the plasma membrane, mitochondrial membrane and secretory vesicles in diverse kinds of cells, belongs to a type of cation translocators. NCX works in two modes, the forward mode and reverse mode. Exactly through the two-way modes, NCX can regulate intracellular Ca2+ concentration fleetly and accurately, and plays a critical role in a series of physiological processes. However, abnormal activation of the reverse mode of NCX plays a vital role in renal ischemia reperfusion injury, which can mediate the overload of cytoplasmic Ca2+, then triggers a series of harmful metabolic reactions that led to cell injury and death. Currently, phenoxyl derivatives that selectively inhibit the reverse mode of NCX have been extensively studied and become new drug targets for the treatment of renal ischemia reperfusion injury.