miR-22 in cardiac remodeling and disease

Abstract

Regulation of gene expression during cardiac development and remodeling is very complicated, involving epigenetic, transcriptional, post-transcriptional, and translational regulation. Our understanding of the molecular mechanisms underlying cardiac remodeling is still far from complete. MicroRNAs are a class of small non-coding RNAs that have been shown to play critical roles in gene regulation in cardiovascular biology and disease. microRNA-22 (miR-22) is an evolutionally conserved miRNA that is highly expressed in the heart. Recent studies uncovered miR-22 as an important regulator for cardiac remodeling. miR-22 modulates the expression and function of genes involved in hypertrophic response, sarcomere reorganization, and metabolic program shift during cardiac remodeling. In this review, we will focus on the recent findings of miR-22 in cardiac remodeling and the therapeutic potential of this miRNA in the treatment of related defects resulting from adverse cardiac remodeling.

Figure 1

Schematic depiction of miR-22 function in the regulation of cardiac remodeling. A transverse view of heart, indicated by the green dashed line in the heart model, is used to show the functional role of miR-22 in cardiac remodeling, including cardiac hypertrophy, dilated cardiomyopathy and fibrosis. The red areas in the ventricle wall of the dilated heart designate fibrosis lesions.

Figure 2

Schematic depiction of miR-22 function in cardiomyocytes. Several miR-22 targets (PurB, Sirt1, etc) and regulatory biological processes (Contraction and metabolism) are highlighted. Ac: acetyl groups; H: histone; HDAC4: histone deacetylase 4; MyoCD: myocardin; PGC-1〈: peroxisome proliferator-activated receptor gamma, coactivator 1 alpha; PPAR〈: peroxisome proliferator activated receptor alpha; PurB: purine rich element binding protein B; Sirt1: sirtuin 1; SRF: serum response factor.