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首页> 外文期刊>Cell and Tissue Research >Regulators of mitochondrial Ca2+ homeostasis in cerebral ischemia
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Regulators of mitochondrial Ca2+ homeostasis in cerebral ischemia

机译：线粒体Ca2 +稳态在脑缺血中的调节剂

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摘要

Cerebral ischemia is a key pathophysiological feature of various brain insults. Inadequate oxygen supply can manifest regionally in stroke or as a result of traumatic brain injury or globally following cardiac arrest, all leading to irreversible brain damage. Mitochondrial function is essential for neuronal survival, since neurons critically depend on ATP synthesis generated by mitochondrial oxidative phosphorylation. Mitochondrial activity depends on Ca2+ and is fueled either by Ca2+ from the extracellular space when triggered by neuronal activity or by Ca2+ released from the endoplasmic reticulum (ER) and taken up through specialized contact sites between the ER and mitochondria known as mitochondrial-associated ER membranes. The coordination of these Ca2+ pools is required to synchronize mitochondrial respiration rates and ATP synthesis to physiological demands. In this review, we discuss the role of the proteins involved in mitochondrial Ca2+ homeostasis in models of ischemia. The proteins include those important for the Ca2+-dependent motility of mitochondria and for Ca2+ transfer from the ER to mitochondria, the tethering proteins that bring the two organelles together, inositol 1,4,5-triphosphate receptors that enable Ca2+ release from the ER, voltage-dependent anion channels that allow Ca2+ entry through the highly permeable outer mitochondrial membrane and the mitochondrial Ca2+ uniporter together with its regulatory proteins that permit Ca2+ entry into the mitochondrial matrix. Finally, we address those proteins important for the extrusion of Ca2+ from the mitochondria such as the mitochondrial Na+/Ca2+ exchanger or, if the mitochondrial Ca 2+ concentration exceeds a certain threshold, the mitochondrial permeability transition pore.
机译：脑缺血是各种脑损伤的关键病理生理特征。氧供应不足可局部发生在中风中，或者是颅脑外伤的结果，或者是心脏骤停后的整体结果，所有这些都会导致不可逆的脑损伤。线粒体功能对于神经元生存至关重要，因为神经元严重依赖于线粒体氧化磷酸化产生的ATP合成。线粒体的活性取决于Ca2 +，并由神经元活性触发时由细胞外空间中的Ca2 +推动，或由内质网（ER）释放并通过ER与线粒体之间的专门接触位点吸收的Ca2 +促进，这称为线粒体相关ER膜。这些Ca2 +库的协调是使线粒体呼吸速率和ATP合成与生理需求同步所必需的。在这篇综述中，我们讨论了参与缺血模型的线粒体Ca2 +稳态蛋白的作用。这些蛋白质包括对于依赖Ca2 +的线粒体运动以及从ER到线粒体的Ca2 +转移，将两个细胞器聚集在一起的束缚蛋白质，肌醇1,4,5-三磷酸受体能够使Ca2 +从ER释放的重要蛋白质。电压依赖性阴离子通道，可允许Ca2 +通过高渗透性线粒体外膜和线粒体Ca2 +单向转运蛋白及其调控蛋白，允许Ca2 +进入线粒体基质。最后，我们讨论了对于从线粒体中挤出Ca2 +的重要蛋白质，例如线粒体Na + / Ca2 +交换子，或者，如果线粒体Ca 2+的浓度超过某个阈值，则线粒体通透性过渡孔。

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