MicroRNAs Regulate Mitochondrial Function in Cerebral Ischemia-Reperfusion Injury

被引:91
作者
Hu, Yue [1 ]
Deng, Hao [2 ]
Xu, Shixin [2 ]
Zhang, Junping [2 ]
机构
[1] Tianjin Univ Tradit Chinese Med, Grad Sch, Tianjin 300193, Peoples R China
[2] Tianjin Univ Tradit Chinese Med, Ctr Med Expt, Teaching Hosp 1, Tianjin 300193, Peoples R China
关键词
ischemic-reperfusion; mitochondria; miRNAs; cerebral; NEURONAL CELL-DEATH; OXIDATIVE STRESS; CYTOCHROME-C; POSTTRANSCRIPTIONAL REGULATION; PERMEABILITY TRANSITION; MOLECULAR-MECHANISMS; TRANSCRIPTION FACTOR; CALCIUM UNIPORTER; DOWN-REGULATION; ROS PRODUCTION;
D O I
10.3390/ijms161024895
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
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.
引用
收藏
页码:24895 / 24917
页数:23
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