Abstract
An increase in stress-associated microRNAs has been observed in the heart after an induced myocardial infarction. Liu and colleagues now demonstrate that one of these stress-associated microRNAs, miR-223-3p, can regulate a component of the voltage-gated channel that mediates rapid outward efflux of potassium during an action potential. Aberrations in the potassium current have been associated with ventricular arrhythmia and heart disease. Strikingly, introducing a small RNA antagonist directed against miR-223-3p into rat hearts, while also inducing a myocardial infarction, resulted in a reduction in arrhythmias. We place these studies in the larger context of the field and discuss the potential of anti-miR-223-3p molecules as new therapeutics for myocardial infarction.