Fibroblast‐derived exosomes enriched with miR‐27a are transported into cardiomyocytes, where they inhibit PDLIM5 expression and exacerbate cardiac hypertrophy in MI‐induced CHF models, a process closely linked to oxidative stress, which significantly contributes to cardiomyocyte dysfunction and myocardial hypertrophy in CHF [63]. This evidence concerns the gene PDLIM5 and cardiac hypertrophy.