Emodin and emodin-rich rhubarb inhibits histone deacetylase (HDAC) activity and cardiac myocyte hypertrophy

Pathological cardiac hypertrophy is a classical hallmark of heart failure. At the molecular level, inhibition of histone deacetylase (HDAC) enzymes attenuate pathological cardiac hypertrophy in vitro and in vivo. Emodin is an anthraquinone that has been implicated in cardiac protection. However, it...

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Veröffentlicht in:	The Journal of nutritional biochemistry 2020-05, Vol.79, p.108339-108339, Article 108339
Hauptverfasser:	Evans, Levi W., Bender, Abigail, Burnett, Leah, Godoy, Luis, Shen, Yi, Staten, Dante, Zhou, Tong, Angermann, Jeffrey E., Ferguson, Bradley S.
Format:	Artikel
Sprache:	eng
Schlagworte:	acetates Acetylation angiotensin II Angiotensin II - pharmacology animal disease models Animals Animals, Newborn Cardiac hypertrophy Cardiomegaly - drug therapy Cardiomegaly - metabolism cardiomyocytes Cardiotonic Agents - pharmacology Disease Models, Animal Emodin Emodin - pharmacology enzyme inhibition Female fibrosis Food bioactives gene expression Gene Expression - drug effects gene expression regulation HDAC Heart failure Histone deacetylase Histone Deacetylase Inhibitors - pharmacology Histone Deacetylases - genetics Histone Deacetylases - metabolism histones Humans Hydroxamic Acids - pharmacology hypertrophy Male Mice Mice, Inbred C57BL Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism phenylephrine Rats Rats, Sprague-Dawley Rheum - chemistry rhubarb
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