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.
Bibliographical noteFunding Information:
I thank Dr. Elizabeth Murphy and Dr. Toren Finkel for helpful discussions and feedback. This work was supported by National Institutes of Health (NIH) grant 1K22HL137901 .
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