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Sulforaphane suppresses cardiac hypertrophy by inhibiting GATA4/GATA6 expression and MAPK signaling pathways
Author(s) -
Kee Hae Jin,
Kim Gwi Ran,
Kim In Kyeom,
Jeong Myung Ho
Publication year - 2015
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201400279
Subject(s) - gata4 , sulforaphane , atrial natriuretic peptide , npr1 , signal transduction , transcription factor , brain natriuretic peptide , muscle hypertrophy , mapk/erk pathway , natriuretic peptide , medicine , endocrinology , biology , cancer research , microbiology and biotechnology , chemistry , biochemistry , gene , heart failure
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.