Suppression of Class I and II Histone Deacetylases Blunts Pressure-Overload Cardiac Hypertrophy | Zendy

Yongli Kong | Zendy; Paul Tannous | Zendy; Guangrong Lu | Zendy; Kambeez Berenji | Zendy; Beverly A. Rothermel | Zendy; Eric N. Olson | Zendy; Joseph A. Hill | Zendy

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Suppression of Class I and II Histone Deacetylases Blunts Pressure-Overload Cardiac Hypertrophy

Author(s) -

Yongli Kong,

Paul Tannous,

Guangrong Lu,

Kambeez Berenji,

Beverly A. Rothermel,

Eric N. Olson,

Joseph A. Hill

Publication year - 2006

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.106.625467

Subject(s) - medicine , pressure overload , muscle hypertrophy , histone , cardiac function curve , cell growth , ventricular remodeling , endocrinology , apoptosis , cardiology , heart failure , cardiac hypertrophy , biology , gene , biochemistry , genetics

Recent work has demonstrated the importance of chromatin remodeling, especially histone acetylation, in the control of gene expression in the heart. In cell culture models of cardiac hypertrophy, pharmacological suppression of histone deacetylases (HDACs) can either blunt or amplify cell growth. Thus, HDAC inhibitors hold promise as potential therapeutic agents in hypertrophic heart disease.

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