The uptake of Ca2+ into mitochondria is thought to be an important signal communicating the need for increased energy production. However, dysregulated uptake leading to mitochondrial Ca2+ overload can trigger opening of the mitochondrial permeability transition pore and potentially cell death. Thus mitochondrial Ca2+ entry is regulated via the activity of a Ca2+-selective channel known as the mitochondrial calcium uniporter. The last decade has seen enormous momentum in the discovery of the molecular identities of the multiple proteins comprising the uniporter. Increasing numbers of studies in cultured cells and animal models have provided insight into how disruption of uniporter proteins affects mitochondrial Ca2+ regulation and impacts tissue function and physiology. This review aims to summarize some of these recent findings, particularly in the context of the heart.

中文翻译：

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MCU对于正常的心脏功能来说是可有可无的吗？


线粒体对 Ca2+ 的吸收被认为是传达增加能量产生需求的重要信号。然而，导致线粒体 Ca2+ 超载的摄取失调可能会触发线粒体通透性转换孔的打开并可能导致细胞死亡。因此，线粒体 Ca2+ 进入是通过称为线粒体钙单向转运蛋白的 Ca2+ 选择性通道的活性来调节的。过去十年，构成单向转运蛋白的多种蛋白质的分子特性的发现取得了巨大的进展。越来越多的培养细胞和动物模型研究深入了解单向转运蛋白的破坏如何影响线粒体 Ca2+ 调节以及组织功能和生理学。这篇综述旨在总结一些最近的发现，特别是在心脏方面。