Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis.

ABSTRACT: Acute myocardial infarction (MI) due to coronary artery occlusion is accompanied by a pathological remodeling response that includes hypertrophic cardiac growth and fibrosis, which impair cardiac contractility. Previously, we showed that cardiac hypertrophy and heart failure are accompanied by characteristic changes in the expression of a collection of specific microRNAs (miRNAs), which act as negative regulators of gene expression. Here, we show that MI in mice and humans also results in the dysregulation of specific miRNAs, which are similar to but distinct from those involved in hypertrophy and heart failure. Among the MI-regulated miRNAs are members of the miR-29 family, which are down-regulated in the region of the heart adjacent to the infarct. The miR-29 family targets a cadre of mR

SUBMITTER: van Rooij E 

PROVIDER: S-EPMC2529064 | biostudies-literature | 2008 Sep

REPOSITORIES: biostudies-literature