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Review
. 2015 Oct 20;16(10):24895-917.
doi: 10.3390/ijms161024895.

MicroRNAs Regulate Mitochondrial Function in Cerebral Ischemia-Reperfusion Injury

Yue Hu  1 , Hao Deng  2 , Shixin Xu  3 , Junping Zhang  4
Affiliations
Review

MicroRNAs Regulate Mitochondrial Function in Cerebral Ischemia-Reperfusion Injury

Yue Hu et al. Int J Mol Sci. .

Abstract

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.

Keywords: cerebral; ischemic-reperfusion; miRNAs; mitochondria.

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Figures

Figure 1
Figure 1
Regulatory role of miRNAs in mitochondrial oxidative stress during brain ischemia-reperfusion injury.
Figure 2
Figure 2
Energy metabolism in the mitochondria during cerebral ischemia-reperfusion injury and the regulatory role of miRNAs.
Figure 3
Figure 3
Apoptosis under pathological conditions of reperfusion and the regulatory roles of miRNAs.
See this image and copyright information in PMC

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