한빛사 논문
Abstract
Hae Jin Kee1,*, Gwi Ran Kim1, In Kyeom Kim2 and Myung Ho Jeong1,†
1 Cardiovascular Convergence Research Center, Chonnam National University Hospital, Gwangju, South Korea
2 Department of Pharmacology, Cardiovascular Research Institute, Kyungpook National University School of Medicine, Daegu, South Korea
† Additional corresponding author: Dr. Myung Ho Jeong
*Correspondence: Dr. Hae Jin Kee, Cardiovascular Convergence Research Center, Chonnam National University Hospital, 42 Jebong-ro, Dong-gu, Gwangju 501-757, South Korea
Abstract
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
논문정보
관련 링크
연구자 키워드
연구자 ID
관련분야 연구자보기
소속기관 논문보기
관련분야 논문보기
해당논문 저자보기