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Life after the birth of the mitochondrial Na+/Ca2+ exchanger, NCLX

机译：线粒体Na + / Ca2 +交换子NCLX出生后的生活

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Powered by the mitochondrial membrane potential, Ca2+ permeates the mitochondria via a Ca2+ channel termed Ca2+ uniporter and is pumped out by a Na+/Ca2+ exchanger, both of which are located on the inner mitochondrial membrane. Mitochondrial Ca2+ transients are critical for metabolic activity and regulating global Ca2+ responses. On the other hand, failure to control mitochondrial Ca2+ is a hallmark of ischemic and neurodegenerative diseases. Despite their importance, identifying the uniporter and exchanger remains elusive and their inhibitors are non-specific. This review will focus on the mitochondrial exchanger, initially describing how it was molecularly identified and linked to a novel member of the Na+/Ca2+ exchanger superfamily termed NCLX. Molecular control of NCLX expression provides a selective tool to determine its physiological role in a variety of cell types. In lymphocytes, NCLX is essential for refilling the endoplasmic reticulum Ca2+ stores required for antigendependent signaling. Communication of NCLX with the store-operated channel in astroglia controls Ca2+ influx and thereby neuro-transmitter release and cell proliferation. The refilling of the Ca2+ stores in the sarcoplasmic reticulum, which is controlled by NCLX, determines the frequency of action potential and Ca2+ transients in cardiomyocytes. NCLX is emerging as a hub for integrating glucose-dependent Na+ and Ca2+ signaling in pancreatic β cells, and the specific molecular control of NCLX expression resolved the controversy regarding its role in neurons and β cells. Future studies on an NCLX knockdown mouse model and identification of human NCLX mutations are expected to determine the role of mitochondrial Ca2+ efflux in organ activity and whether NCLX inactivation is linked to ischemic and/or neurodegenerative syndromes. Structure-function analysis and protein analysis will identify the NCLX mode of regulation and its partners in the inner membrane of the mitochondria. Keywords NCLX MCU mitochondrial Ca2+ signaling Na+/Ca2+ exchanger Na+ signaling.
机译：在线粒体膜电位的驱动下，Ca 2 + 通过称为Ca 2 + 单向转运体的Ca 2 + 通道渗透到线粒体，并被泵出Na + / Ca 2 + 交换剂，两者均位于线粒体内膜上。线粒体Ca 2 + 瞬变对于代谢活动和调节整体Ca 2 + 反应至关重要。另一方面，无法控制线粒体Ca 2 + 是缺血性和神经退行性疾病的标志。尽管它们很重要，但仍然难以确定单向转运蛋白和交换子，并且它们的抑制剂是非特异性的。这篇综述将集中于线粒体交换子，最初描述它是如何被分子鉴定并与Na + / Ca 2 + 交换子超家族的新成员NCLX连接的。 NCLX表达的分子控制为确定其在多种细胞类型中的生理作用提供了一种选择性工具。在淋巴细胞中，NCLX对于补充依赖抗原的信号所需的内质网Ca 2 + 储存至关重要。 NCLX与星形胶质细胞中的存储操纵通道的通信控制Ca 2 + 的流入，从而控制神经递质的释放和细胞增殖。 NCLX控制的肌浆网中Ca 2 + 储库的重新填充决定了心肌细胞中动作电位和Ca 2 + 瞬变的频率。 NCLX逐渐成为整合胰岛β细胞中葡萄糖依赖性Na + 和Ca 2 + 信号转导的枢纽，并且NCLX表达的特异性分子控制解决了有关其的争议在神经元和β细胞中的作用。 NCLX基因敲除小鼠模型的未来研究和人类NCLX突变的鉴定有望确定线粒体Ca 2 + 外排在器官活动中的作用，以及NCLX失活是否与缺血性和/或神经退行性综合症有关。结构功能分析和蛋白质分析将确定线粒体内膜的NCLX调节模式及其伴侣。关键词NCLX MCU线粒体Ca 2 + 信号传导Na + / Ca 2 + 交换子Na + 信号传导。

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