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Modulation of the cardiac Na+-Ca2+ exchanger by cytoplasmic protons: Molecular mechanisms and physiological implications.
Cell Calcium ( IF 4.3 ) Pub Date : 2019-12-11 , DOI: 10.1016/j.ceca.2019.102140 Kyle Scranton 1 , Scott John 2 , Ariel Escobar 3 , Joshua I Goldhaber 4 , Michela Ottolia 5
Cell Calcium ( IF 4.3 ) Pub Date : 2019-12-11 , DOI: 10.1016/j.ceca.2019.102140 Kyle Scranton 1 , Scott John 2 , Ariel Escobar 3 , Joshua I Goldhaber 4 , Michela Ottolia 5
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A precise temporal and spatial control of intracellular Ca2+ concentration is essential for a coordinated contraction of the heart. Following contraction, cardiac cells need to rapidly remove intracellular Ca2+ to allow for relaxation. This task is performed by two transporters: the plasma membrane Na+-Ca2+ exchanger (NCX) and the sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA). NCX extrudes Ca2+ from the cell, balancing the Ca2+entering the cytoplasm during systole through L-type Ca2+ channels. In parallel, following SR Ca2+ release, SERCA activity replenishes the SR, reuptaking Ca2+ from the cytoplasm. The activity of the mammalian exchanger is fine-tuned by numerous ionic allosteric regulatory mechanisms. Micromolar concentrations of cytoplasmic Ca2+ potentiate NCX activity, while an increase in intracellular Na+ levels inhibits NCX via a mechanism known as Na+-dependent inactivation. Protons are also powerful inhibitors of NCX activity. By regulating NCX activity, Ca2+, Na+ and H+ couple cell metabolism to Ca2+ homeostasis and therefore cardiac contractility. This review summarizes the recent progress towards the understanding of the molecular mechanisms underlying the ionic regulation of the cardiac NCX with special emphasis on pH modulation and its physiological impact on the heart.
中文翻译：
细胞质子对心脏Na + -Ca2 +交换子的调节：分子机制和生理意义。
细胞内Ca2 +浓度的精确时空控制对于心脏的协调收缩至关重要。收缩后，心脏细胞需要迅速去除细胞内Ca2 +，以使其放松。此任务由两个转运蛋白执行：质膜Na + -Ca2 +交换剂（NCX）和肌浆网（SR）Ca2 + -ATPase（SERCA）。NCX从细胞中挤出Ca2 +，从而在收缩期通过L型Ca2 +通道平衡Ca2 +进入细胞质。同时，在SR Ca2 +释放后，SERCA活性补充了SR，从细胞质中重新吸收了Ca2 +。哺乳动物交换子的活性通过多种离子变构调节机制进行了微调。细胞质Ca2 +的微摩尔浓度可增强NCX活性，而细胞内Na +水平的升高则通过一种称为Na +依赖性失活的机制抑制NCX。质子还是NCX活性的强大抑制剂。通过调节NCX活性，Ca2 +，Na +和H +将细胞代谢与Ca2 +稳态结合，从而使心脏收缩。这篇综述总结了对理解心脏NCX离子调节的分子机制的最新进展，其中特别强调了pH调节及其对心脏的生理影响。
更新日期：2019-12-11
中文翻译：
细胞质子对心脏Na + -Ca2 +交换子的调节：分子机制和生理意义。
细胞内Ca2 +浓度的精确时空控制对于心脏的协调收缩至关重要。收缩后，心脏细胞需要迅速去除细胞内Ca2 +，以使其放松。此任务由两个转运蛋白执行：质膜Na + -Ca2 +交换剂（NCX）和肌浆网（SR）Ca2 + -ATPase（SERCA）。NCX从细胞中挤出Ca2 +，从而在收缩期通过L型Ca2 +通道平衡Ca2 +进入细胞质。同时，在SR Ca2 +释放后，SERCA活性补充了SR，从细胞质中重新吸收了Ca2 +。哺乳动物交换子的活性通过多种离子变构调节机制进行了微调。细胞质Ca2 +的微摩尔浓度可增强NCX活性，而细胞内Na +水平的升高则通过一种称为Na +依赖性失活的机制抑制NCX。质子还是NCX活性的强大抑制剂。通过调节NCX活性，Ca2 +，Na +和H +将细胞代谢与Ca2 +稳态结合，从而使心脏收缩。这篇综述总结了对理解心脏NCX离子调节的分子机制的最新进展，其中特别强调了pH调节及其对心脏的生理影响。
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