MicroRNAs Regulate Mitochondrial Function in Cerebral Ischemia-Reperfusion Injury.
MicroRNAs Regulate Mitochondrial Function in Cerebral Ischemia-Reperfusion Injury.
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MicroRNAs 调节脑缺血再灌注损伤中的线粒体功能
DOI：
10.3390/ijms161024895
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发表时间：
2015-10-20
影响因子：
5.6
通讯作者：
Zhang J
中科院分区：
文献类型：
--
作者：
Hu Y;Deng H;Xu S;Zhang J
脑缺血再灌注损伤涉及线粒体内多条独立致死的末端通路。这些途径包括线粒体膜电位变化和钙超载引起的活性氧(ROS)的产生，通过细胞色素c(Cytc)的释放导致细胞凋亡。此外，许多microRNAs与整个过程有关。在这篇综述中，我们首先简要总结了脑缺血再灌注时线粒体的变化，然后描述了miRNA调节线粒体功能的可能的分子机制，其中可能包括氧化应激和能量代谢，以及细胞凋亡。在上述分析的基础上，我们得出结论，对调控线粒体功能的microRNAs的研究将加速脑缺血再灌注损伤治疗的发展。
Cerebral ischemia-reperfusion injury involves multiple independently fatal terminal pathways in the mitochondria. These pathways include the reactive oxygen species (ROS) generation caused by changes in mitochondrial membrane potential and calcium overload, resulting in apoptosis via cytochrome c (Cyt c) release. In addition, numerous microRNAs are associated with the overall process. In this review, we first briefly summarize the mitochondrial changes in cerebral ischemia-reperfusion and then describe the possible molecular mechanism of miRNA-regulated mitochondrial function, which likely includes oxidative stress and energy metabolism, as well as apoptosis. On the basis of the preceding analysis, we conclude that studies of microRNAs that regulate mitochondrial function will expedite the development of treatments for cerebral ischemia-reperfusion injury.