Scope: Sulforaphane (SFN) is a naturally occurring isothiocynate compound found in cruciferous vegetables. Here, we report the effect of SFN on cardiac hypertrophy and propose an underlying mechanism.
Methods and results: SFN suppresses cardiomyocyte hypertrophy induced by hypertrophic stimuli in vitro and in vivo. SFN suppresses the expression of fetal genes, including atrial natriuretic peptide, brain natriuretic peptide, and beta myosin heavy chain. We used an siRNA technique and atrial natriuretic peptide promoter with mutated GATA binding sites to demonstrate that SFN mediates cardiac hypertrophy by modulating transcription factors GATA4/6.
Conclusion: These results suggest that SFN has the potential to prevent cardiac hypertrophy by downregulating GATA4/6 and mitogen-activated protein kinase signaling pathways.
Keywords: Cardiac hypertrophy; GATA binding factor 4; GATA binding factor 6; Mitogen-activated protein kinase signaling; Sulforaphane.
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