Energy metabolism impairment is a central event in the pathophysiology of ischemia. The limited availability of glucose and oxygen strongly affects mitochondrial activity, thus leading to ATP depletion. In this setting, the switch to alternative energy sources could ameliorate cells survival by enhancing ATP production, thus representing an attractive strategy for ischemic treatment. In this regard, some studies have recently re-evaluated the metabolic role of glutamate and its potential to promote cell survival under pathological conditions. In the present review, we discuss the ability of glutamate to exert an "energizing role" in cardiac and neuronal models of hypoxia/reoxygenation (H/R) injury, focusing on the Na+/Ca2+ exchanger (NCX) and the Na+-dependent excitatory amino acid transporters (EAATs) as key players in this metabolic pathway.

中文翻译：

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缺血中的NCX和EAAT转运蛋白：处于谷氨酸代谢和细胞存活之间的十字路口。

能量代谢障碍是缺血的病理生理中的中心事件。葡萄糖和氧气的有限可用性会严重影响线粒体活性，从而导致ATP耗竭。在这种情况下，转向替代能源可以通过增强ATP的产生来改善细胞的存活率，从而代表了一种有吸引力的缺血治疗策略。在这方面，最近的一些研究重新评估了谷氨酸的代谢作用及其在病理条件下促进细胞存活的潜力。在本综述中，我们讨论了谷氨酸在缺氧/复氧（H / R）损伤的心脏和神经元模型中发挥“激发作用”的能力，