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Significance Heart failure is a major cause of mortality in humans. In a heart failure model induced by pressure overloading, we previously reported that the RNA binding protein RBFox2 was greatly diminished, leading to impaired excitation–contraction (EC) coupling. We have now pursued the mechanism for RBFox2 ablation-induced EC-coupling defects, revealing that RBFox2 depletion and resultant cardiac stress induce a set of microRNAs, including miR-34a, which directly targets the critical EC couplerJph2 to further stress the heart. Significantly, systematic administration of a miR-34a antagomir is able to attenuate RBFox2 ablation-induced heart failure. These findings suggest a critical role of the RBFox2-miR-34a-Jph2 axis in causing progressive failure, which may be therapeutically intervened with a microRNA antagomir.

RBFox2-miR-34a-Jph2 axis contributes to cardiac decompensation during heart failure