Our study suggested that SFI attenuated myocardial hypertrophy probably by enhancing the expression of miR-19a-3p and down-regulating the expression of MEF2A, β-MHC, BNP and TRPC1, which seemingly implies that the SFI mediated improvement within MEF2 signaling might be the cause of attenuated myocardial hypertrophy. This evidence concerns the gene TRPC1 and cardiac hypertrophy.