Department of Biomedical Sciences, University of Padova, Italy.
Department of Biomedical Sciences, University of Padova, Italy.
Cell Calcium. 2018 Jan;69:73-80. doi: 10.1016/j.ceca.2017.08.008. Epub 2017 Aug 25.
During the 60s, the notion that positively charged Ca ions are rapidly accumulated in energized mitochondria has been first established. In the following decades, mitochondrial Ca homeostasis was shown to control cell metabolism, cell survival and other cell-specific functions through different mechanism. However, the molecular identity of the molecules controlling this process remained a mystery until just few years ago, when both mitochondrial Ca uptake and release systems were genetically dissected. This finally opened the possibility to develop genetic model to directly test the contribution of mitochondrial Ca homeostasis to cellular functions. Although the picture is still far from being clear, we here summarize and critically evaluate the current knowledge on how mitochondrial Ca handling controls cell death.
在 20 世纪 60 年代，人们首次提出带正电荷的钙离子迅速积累在充满能量的线粒体中的观点。在接下来的几十年里，通过不同的机制，线粒体钙稳态被证明可以控制细胞代谢、细胞存活和其他细胞特异性功能。然而，直到几年前，当线粒体钙摄取和释放系统被基因解析时，控制这一过程的分子的分子身份仍然是一个谜。这最终为开发遗传模型以直接测试线粒体钙稳态对细胞功能的贡献提供了可能性。尽管目前的情况还远不清楚，但我们在这里总结和批判性地评估了当前关于线粒体钙处理如何控制细胞死亡的知识。
