It has been demonstrated for more than 40 years that intracellular calcium (Ca^2 +) controls a variety of cellular functions, including mitochondrial metabolism and cell proliferation. Cytosolic Ca^2 + fluctuation during key stages of the cell cycle can lead to mitochondrial Ca^2 + uptake and subsequent activation of mitochondrial oxidative phosphorylation and a range of signaling. However, the relationship between mitochondrial Ca^2 + and cell cycle progression has long been neglected because the molecule responsible for Ca^2 + uptake has been unknown. Recently, the identification of the mitochondrial Ca^2 + uniporter (MCU) has led to key advances. With improved Ca^2 + imaging and detection, effects of MCU-mediated mitochondrial Ca^2 + have been observed at different stages of the cell cycle. Elevated Ca^2 + signaling boosts ATP and ROS production, remodels cytosolic Ca^2 + pathways and reprograms cell fate-determining networks. These findings suggest that manipulating mitochondrial Ca^2 + signaling may serve as a potential strategy in the control of many crucial biological events, such as tumor development and cell division in hematopoietic stem cells (HSCs). In this review, we summarize the current understanding of the role of mitochondrial Ca^2 + signaling during different stages of the cell cycle and highlight the potential physiological and pathological significance of mitochondrial Ca^2 + signaling.

40 多年来，细胞内钙 (Ca ^{2  +} ) 已被证明可以控制多种细胞功能，包括线粒体代谢和细胞增殖。细胞周期关键阶段的细胞溶质 Ca ^{2  +波动可导致线粒体 Ca 2  +}摄取和随后激活线粒体氧化磷酸化和一系列信号传导。^{然而，线粒体Ca 2  +}与细胞周期进程之间的关系长期以来一直被忽视，因为负责Ca ^{2  +}摄取的分子一直未知。最近，线粒体 Ca ^{2  +}uniporter (MCU) 取得了重大进展。随着 Ca ^{2  +}成像和检测的改进，已在细胞周期的不同阶段观察到MCU 介导的线粒体 Ca ^{2  +效应。}升高的 Ca ^{2  +}信号可促进 ATP 和 ROS 的产生，重塑细胞溶质 Ca ^{2  +}通路并重新编程决定细胞命运的网络。这些发现表明，操纵线粒体 Ca ^{2  +}信号可能作为控制许多关键生物学事件的潜在策略，例如造血干细胞 (HSC) 中的肿瘤发展和细胞分裂。在这篇综述中，我们总结了目前对线粒体 Ca 的作用的理解。^{2  +}信号在细胞周期的不同阶段，并突出线粒体 Ca ^{2  +}信号的潜在生理和病理意义。