Mitochondrial-mediated suppression of ROS production upon exposure of neurons to lethal stress: mitochondrial targeted preconditioning.
Mitochondrial-mediated suppression of ROS production upon exposure of neurons to lethal stress: mitochondrial targeted preconditioning.
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DOI：
10.1016/j.addr.2008.03.020
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发表时间：
2008-10
影响因子：
16.1
通讯作者：
Bari, Ferenc
中科院分区：
文献类型：
--
作者：
Busija, David W.;Gaspar, Tamas;Domoki, Ferenc;Katakam, Prasad V.;Bari, Ferenc
关键词：
预处理代表细胞短暂暴露于起始事件导致对随后的潜在致死刺激的保护的条件。近年来的研究表明，神经元为中心的机制是促进预适应反应发展的重要介质。然而，关于这些机制的许多细节尚不清楚。这篇综述的目的是描述启动和随后的细胞内事件涉及线粒体，可以导致神经元预处理。这些线粒体特异性靶标包括：1）位于线粒体内膜上的钾通道; 2）呼吸链酶;和3）氧化磷酸化。线粒体ATP敏感性钾（mitoKATP）通道激活和/或呼吸链中断后或能量底物剥夺期间活性氧（ROS）产生增加后，涉及蛋白激酶的形态学变化或信号传导事件对神经元赋予立即或延迟的预处理，使其能够在其他致命损伤中存活。虽然所涉及的机制还不确定，但预处理的结果是在应激期间和应激后增强活力，减弱细胞内钙的流入，降低ROS的可用性，抑制细胞凋亡和维持ATP水平。
Preconditioning represents the condition where transient exposure of cells to an initiating event leads to protection against subsequent, potentially lethal stimuli. Recent studies have established that mitochondrial-centered mechanisms are important mediators in promoting development of the preconditioning response. However, many details concerning these mechanisms are unclear. The purpose of this review is to describe the initiating and subsequent intracellular events involving mitochondria which can lead to neuronal preconditioning. These mitochondrial specific targets include: 1) potassium channels located on the inner mitochondrial membrane; 2) respiratory chain enzymes; and 3) oxidative phosphorylation. Following activation of mitochondrial ATP-sensitive potassium (mitoKATP) channels and/or increased production of reactive oxygen species (ROS) following disruption of the respiratory chain or during energy substrate deprivation, morphological changes or signaling events involving protein kinases confer immediate or delayed preconditioning on neurons that will allow them to survive otherwise lethal insults. While the mechanisms involved are not known with certainty, the results of preconditioning are the enhanced viability, the attenuated influx of intracellular calcium, the reduced availability of ROS, suppression of apoptosis, and the maintenance of ATP levels during and following stress.
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