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.