Role of microRNAs in the reperfused myocardium towards post-infarct remodelling.

Myocardial ischaemia/reperfusion (I/R)-induced remodelling generally includes cell death (necrosis and apoptosis), myocyte hypertrophy, angiogenesis, cardiac fibrosis, and myocardial dysfunction. It is becoming increasingly clear that microRNAs (miRNAs or miRs), a group of highly conserved small (∼18-24 nucleotide) non-coding RNAs, fulfil specific functions in the reperfused myocardium towards post-infarct remodelling. While miR-21, -133, -150, -195, and -214 regulate cardiomyocyte hypertrophy, miR-1/-133 and miR-208 have been elucidated to influence myocardial contractile function. In addition, miR-21, -24, -133, -210, -494, and -499 appear to protect myocytes against I/R-induced apoptosis, whereas miR-1, -29, -199a, and -320 promote apoptosis. Myocardial fibrosis can be regulated by the miR-29 family and miR-21. Moreover, miR-126 and miR-210 augment I/R-induced angiogenesis, but miR-24, -92a, and -320 suppress post-infarct neoangiogenesis. In this review, we summarize the latest advances in the identification of myocardial ischaemia-associated miRNAs and their functional significance in the modulation of I/R-triggered remodelling. Controversial effects of some miRNAs in post-infarct remodelling will be also discussed.