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MicroRNAs in cardiac hypertrophy: angels or devils

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Abstract MicroRNAs (miRNAs) are short noncoding RNA molecules that can regulate gene expression via affecting mRNA stability or translation efficiency. miRNAs mediate many important cellular processes and emerge as a newly discovered regulator of gene expression. In cardiac hypertrophy, miRNAs expression is aberrantly altered. Some of these miRNAs can promote cardiac hypertrophy, whereas others can inhibit the process. In this review, we summarize the up‐ and downregulated miRNAs during cardiac hypertrophy and discuss about their roles in cardiac hypertrophy. The studies on miRNAs shed new light on the mechanism of cardiac hypertrophy and suggest that they may be promising therapeutic targets in tackling cardiac hypertrophy. WIREs RNA 2011 2 124–134 DOI: 10.1002/wrna.61 This article is categorized under: RNA in Disease and Development > RNA in Disease

MicroRNAs (miRNAs) can regulate cardiac hypertrophy. miR‐1, miR‐26, and miR‐133 play an anti‐hypertrophic role and they can inhibit hypertrophy (−). miR‐23a, miR‐195, and miR‐208a play a pro‐hypertrophic role and they can promote hypertrophy (+). The exact role of miR‐21 in cardiac hypertrophy remains to be further characterized.

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The expression of microRNAs (miRNAs) can be regulated by transcription factors. Serum response factor (SRF) can promote the expression of miR‐1. However, it is not yet clear whether this regulation is integrated into the hypertrophic machinery. Nuclear factor of activated T cells c3 (NFATc3) can upregulate the expression of miR‐23a that provokes hypertrophy.

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