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J Mol Cell Cardiol. 2014 Sep;74:98-102. doi: 10.1016/j.yjmcc.2014.05.002. Epub 2014 May 14.

BET-ting on chromatin-based therapeutics for heart failure.

Author information

1
Case Cardiovascular Research Institute, Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA; Harrington Heart & Vascular Institute, University Hospitals Case Medical Center, Cleveland, OH 44106, USA. Electronic address: saptarsi.haldar@case.edu.
2
Department of Medicine, Division of Cardiology, University of Colorado Denver, Aurora, CO 80045, USA. Electronic address: timothy.mckinsey@ucdenver.edu.

Abstract

Studies of transcriptional mechanisms in heart failure have focused heavily on roles of sequence-specific DNA-binding factors such as NFAT, MEF2 and GATA4. Recent findings have illuminated crucial functions for epigenetic regulators in the control of cardiac structural remodeling and mechanical dysfunction in response to pathological stress. Here, we review the current understanding of chromatin-dependent signal transduction in cardiac gene control, and highlight the potential for pharmacologic regulation of BET acetyl-lysine binding proteins as a means of treating heart failure.

KEYWORDS:

BET proteins; Cardiac hypertrophy; Chromatin; Epigenetics; Heart failure; Transcription

PMID:
24838003
PMCID:
PMC4115033
DOI:
10.1016/j.yjmcc.2014.05.002
[Indexed for MEDLINE]
Free PMC Article

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