Differential expression of microRNAs in ischemic heart disease

Abstract

Recent studies provide evidence that ischemic preconditioning (IP) and ischemia/reperfusion (IR) injury lead to altered expression of microRNAs (miRNAs) that affect the survival and recovery of cardiomyocytes. These endogenous ∼22-nucleotide noncoding RNAs negatively regulate gene expression via degradation and translational inhibition of their target mRNAs. miRNAs are involved in differentiation, proliferation, electrical conduction, angiogenesis and apoptosis. These pathways can lead to physiological and pathological adaptations. This review intends to explore several facets of miRNA expression and the underlying mechanisms involved in IR injury, as well as IP as a cardioprotective strategy. In addition, we will investigate miRNA interaction with the renin-angiotensin system and the potential use of miRNAs in developing sensitive biomarkers for cardiovascular disease.

Conflict of interest statement

Conflicts of interest

The authors declare no conflicts of interest.

Copyright © 2014 Elsevier Ltd. All rights reserved.

Figures

Figure 1

Schematic representation of miRNA biogenesis. The process includes transcription, pre-miRNA formation, miRNA:miRNA*duplex, mature miRNA and miRNA target mRNA inhibition. This diagram outlines two potential mechanisms for miRNA/mRNA silencing: translational repression and mRNA target cleavage. A detailed discussion of post-transcriptional inhibition is included in the text.

Figure 2

Schematic representation of miRNA and its target mRNA and proteins involved in arrhythmia, cell death and survival. Several miRNAs target mRNA and proteins, which can result in arrhythmia, cell death or cell survival.

Figure 3

Schematic representation of miRNA and its target mRNA and proteins involved in hypertrophy, fibrosis and angiogenesis. Several miRNAs target mRNA and proteins, which can lead to cardiovascular changes via hypertrophy, fibrosis and angiogenesis.