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Cardiac fibrosis occurs because of disruption of the extracellular matrix network leading to myocardial dysfunction. Angiotensin II has been implicated in the development of cardiac fibrosis. Recently, microRNAs have been identified as an attractive target for therapeutic intervention in cardiac pathologies; however, the underlying mechanism of microRNAs in cardiac fibrosis remains unclear. MicroRNA‐130a (miR‐130a) has been shown to participate in angiogenesis and cardiac arrhythmia; however, its role in cardiac fibrosis is unknown.

In this study, we found that miR‐130a was significantly upregulated in angiotensin II‐infused mice. The in vivo inhibition of miR‐130a by locked nucleic acid– based anti‐miR‐130a in mice significantly reduced angiotensin II‐induced cardiac fibrosis. Upregulation of miR‐130a was confirmed in failing human hearts. Overexpressing miR‐130a in …