Hypoxic-ischemic injury in the developing brain: the role of reactive oxygen species originating in mitochondria.
Hypoxic-ischemic injury in the developing brain: the role of reactive oxygen species originating in mitochondria.
复制标题
发育中的大脑中缺氧 - 缺血性损伤：起源于线粒体的活性氧的作用。
DOI：
10.1155/2012/542976
复制
发表时间：
2012
影响因子：
1.5
通讯作者：
Starkov A
中科院分区：
文献类型：
--
作者：
Ten VS;Starkov A
线粒体功能障碍是脑缺氧缺血再灌注损伤的最根本机制。线粒体呼吸链(MRC)被认为是缺血后组织中活性氧(ROS)的来源。起源于MRC的ROS可能有助于再灌流驱动的氧化应激，促进线粒体膜通透性。再灌流过程中线粒体膜完整性的丧失被认为是继发性能量衰竭的主要机制。本文综述了线粒体呼吸链上的ROS在继发性能量衰竭中的致病作用，并提出了针对发育中脑缺氧-缺血-再灌注损伤后再灌注所致氧化应激的潜在治疗策略。
Mitochondrial dysfunction is the most fundamental mechanism of cell damage in cerebral hypoxia-ischemia and reperfusion. Mitochondrial respiratory chain (MRC) is increasingly recognized as a source for reactive oxygen species (ROS) in the postischemic tissue. Potentially, ROS originating in MRC can contribute to the reperfusion-driven oxidative stress, promoting mitochondrial membrane permeabilization. The loss of mitochondrial membranes integrity during reperfusion is considered as the major mechanism of secondary energy failure. This paper focuses on current data that support a pathogenic role of ROS originating from mitochondrial respiratory chain in the promotion of secondary energy failure and proposes potential therapeutic strategy against reperfusion-driven oxidative stress following hypoxia-ischemia-reperfusion injury of the developing brain.