Thus, in vitro findings combined with the in vivo results in the present study uncovered a novel mechanism by which miR‐486 improves fibrotic activity, pathologic remodelling and scar size in MI via an SRSF3 gene silencing‐mediated increase in p21 signalling resulting in cellular senescence of CMFs, which benefits MI regeneration. This evidence concerns the gene SRSF3 and myocardial infarction.