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Review
. 2017 Mar 31;18(4):745.
doi: 10.3390/ijms18040745.

The Role of MicroRNAs in Myocardial Infarction: From Molecular Mechanism to Clinical Application

Teng Sun  1 , Yan-Han Dong  2 , Wei Du  3 , Chun-Ying Shi  4 , Kun Wang  5 , Muhammad-Akram Tariq  6 , Jian-Xun Wang  7 , Pei-Feng Li  8
Affiliations
Review

The Role of MicroRNAs in Myocardial Infarction: From Molecular Mechanism to Clinical Application

Teng Sun et al. Int J Mol Sci. .

Abstract

MicroRNAs (miRNAs) are a class of small single-stranded and highly conserved non-coding RNAs, which are closely linked to cardiac disorders such as myocardial infarction (MI), cardiomyocyte hypertrophy, and heart failure. A growing number of studies have demonstrated that miRNAs determine the fate of the heart by regulating cardiac cell death and regeneration after MI. A deep understanding of the pathophysiology of miRNA dependent regulatory pathways in these processes is required. The role of miRNAs as diagnostic, prognostic, and therapeutic targets also needs to be explored in order to utilize them in clinical settings. This review summarizes the role of miRNAs in myocardial infarction and focuses mainly on their influence on cardiomyocyte regeneration and cell death including apoptosis, necrosis, and autophagy. In addition, the targets of pro- and anti-MI miRNAs are comparatively described. In particular, the possibilities of miRNA-based diagnostic and therapeutic strategies for myocardial infarction are discussed in this review.

Keywords: cardiomyocyte regeneration; clinical application; microRNAs; myocardial cell death; myocardial infarction.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic diagram of miRNA-mediated mRNA translational repression and decay. (a) miRNA-induced silencing coplex (miRISC) prevents the eIF4E-cap recognition and 40S ribosomal subunits recruitment; (b) 60S ribosomal subunit joining is prevented by miRISC; (c) Translation is inhibited by ribosome drop-off; (d) Translation is blocked by nascent polypeptide degradation; (e) miRISC interacts with Poly (A)-binding protein (PABP), CCR4-assocated factor (CAF1), negative on TATA-less (NOT1), and carbon catabolite repression 4 (CCR4), which mediate deadenylation, decapping, and mRNA decay; (f) miRISC interacts with decapping factor DCP1/2 for decapping and mRNA decay. Blue arrows represent the recruitment and disassociation of 40S/60S ribosomal subunits. Orange arrows represent the process fancilited by AGO/GW182. Orange T blocks represent the process prevented by AGO/GW182. Red cross (x), degradation of nascent polypeptide. Red arrows represent the interaction between AGO/GW182 and indicated factors and their function upon miRNA regulation.
Figure 2
Figure 2
Overview of the role of miRNAs-regulated myocardial cell death in MI. See text for detailed explanations. Blue arrows and plus sign indicate that the final effect is the activation of cell death. T bars and minus sign indicates that the final effect is the inhibition of cell death.
Figure 3
Figure 3
Summary of miRNAs functioning to regulate cardiac regeneration in MI. Cardiomyocytes proliferation, cardiac fibroblasts reprogramming and stem/progenitor cells differentiation mediated by miRNAs are shown in the figure. See text for detailed explanations. Both blue and grey arrows represent the promotion effect. T bars represent the inhibition effect.
See this image and copyright information in PMC

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