The ins and outs of mitochondrial calcium.
The ins and outs of mitochondrial calcium.
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DOI：
10.1161/circresaha.116.305484
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发表时间：
2015-05-22
影响因子：
20.1
通讯作者：
Murphy E
中科院分区：
文献类型：
--
作者：
Finkel T;Menazza S;Holmström KM;Parks RJ;Liu J;Sun J;Liu J;Pan X;Murphy E
钙被认为在调节线粒体功能中发挥重要作用。有证据表明，线粒体钙的增加可以通过改变钙敏感线粒体基质酶的活性来增加 ATP 的产生。相反，在缺血再灌注损伤的情况下，大量线粒体钙的进入被认为是引发细胞坏死的关键事件。几十年来，钙如何进入线粒体的细节仍然是一个生物学之谜。在过去的几年中，在鉴定线粒体钙单向转运蛋白复合物的分子成分方面取得了重大进展。在这里，我们回顾了钙如何进入和离开线粒体，对单向转运蛋白复合物的拓扑结构、化学计量和功能的日益深入的了解，以及从一些从遗传上扰乱线粒体钙稳态的最初小鼠模型中吸取的早期教训。
Calcium is thought to play an important role in regulating mitochondrial function. Evidence suggests that an increase in mitochondrial calcium can augment ATP production by altering the activity of calcium-sensitive mitochondrial matrix enzymes. In contrast, the entry of large amounts of mitochondrial calcium in the setting of ischemia-reperfusion injury is believed to be a critical event in triggering cellular necrosis. For many decades, the details of how calcium entered the mitochondria remained a biological mystery. In the last few years, significant progress has been made in identifying the molecular components of the mitochondrial calcium uniporter complex. Here, we review how calcium enters and leaves the mitochondria, the growing insight into the topology, stoichiometry and function of the uniporter complex and the early lessons learned from some initial mouse models that genetically perturb mitochondrial calcium homeostasis.