Store-operated Ca²⁺ entry (SOCE) machinery, including Orai channels, TRPCs, and STIM1, is key to cellular calcium homeostasis. The following characteristics of mitochondria are involved in the physiological and pathological regulation of cells: mitochondria mediate calcium uptake through calcium uniporters; mitochondria are regulated by mitochondrial dynamic related proteins (OPA1, MFN1/2, and DRP1) and form mitochondrial networks through continuous fission and fusion; mitochondria supply NADH to the electron transport chain through the Krebs cycle to produce ATP; under stress, mitochondria will produce excessive reactive oxygen species to regulate mitochondria-endoplasmic reticulum interactions and the related signalling pathways. Both SOCE and mitochondria play critical roles in mediating cardiac hypertrophy, diabetic cardiomyopathy, and cardiac ischaemia-reperfusion injury. All the mitochondrial characteristics mentioned above are determinants of SOCE activity, and vice versa. Ca²⁺ signalling dictates the reciprocal regulation between mitochondria and SOCE under the specific pathological conditions of cardiomyocytes. The coupling of mitochondria and SOCE is essential for various pathophysiological processes in the heart. Herein, we review the research focussing on the reciprocal regulation between mitochondria and SOCE and provide potential interplay patterns in cardiac diseases.

中文翻译：

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线粒体和储存操作的 Ca2+ 进入之间的相互作用：对心脏病的新见解

商店经营的Ca ²⁺进入 (SOCE) 机制，包括 Orai 通道、TRPC 和 STIM1，是细胞钙稳态的关键。线粒体的以下特性参与细胞的生理和病理调节： 线粒体通过钙单向转运体介导钙摄取；线粒体受线粒体动力学相关蛋白（OPA1、MFN1/2和DRP1）的调控，通过不断的裂变和融合形成线粒体网络；线粒体通过克雷布斯循环向电子传递链提供 NADH 以产生 ATP；在压力下，线粒体会产生过多的活性氧来调节线粒体-内质网的相互作用以及相关的信号通路。SOCE 和线粒体在介导心脏肥大、糖尿病性心肌病、和心脏缺血再灌注损伤。上述所有线粒体特征都是 SOCE 活性的决定因素，反之亦然。钙在心肌细胞的特定病理条件下，2 ^{+信号决定了线粒体和 SOCE 之间的相互调节。}线粒体和 SOCE 的耦合对于心脏中的各种病理生理过程至关重要。在此，我们回顾了专注于线粒体和 SOCE 之间相互调节的研究，并提供了心脏病中潜在的相互作用模式。