Moreover, although HCM is a genetic cardiomyocyte-intrinsic disease, there are common pathological changes (such as cardiomyocyte hypertrophy and fibrosis) and common activating signal pathways (such as TGF-β/SMAD3) between HCM and severe aortic stenosis or long-standing hypertension.29,30 Thus, we tested whether mir-27b-3p was up-regulated in hypertrophic heart tissue from patients with HCM. This evidence concerns the gene SMAD3 and aortic stenosis.