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

Abstract:

: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.

journal_name

Cardiovasc Res

journal_title

Cardiovascular research

authors

Zhu H,Fan GC

doi

10.1093/cvr/cvr291

subject

Has Abstract

pub_date

2012-05-01 00:00:00

pages

284-92

issue

2

eissn

0008-6363

issn

1755-3245

pii

cvr291

journal_volume

94

pub_type

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