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F1000Res. 2018 Oct 29;7. pii: F1000 Faculty Rev-1713. doi: 10.12688/f1000research.15797.1. eCollection 2018.

Epigenomic regulation of heart failure: integrating histone marks, long noncoding RNAs, and chromatin architecture.

Author information

1
Department of Medicine, Division of Cardiology and Consortium for Fibrosis Research & Translation, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
2
Departments of Anesthesiology, Medicine, and Physiology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.

Abstract

Epigenetic processes are known to have powerful roles in organ development across biology. It has recently been found that some of the chromatin modulatory machinery essential for proper development plays a previously unappreciated role in the pathogenesis of cardiac disease in adults. Investigations using genetic and pharmacologic gain- and loss-of-function approaches have interrogated the function of distinct epigenetic regulators, while the increased deployment of the suite of next-generation sequencing technologies have fundamentally altered our understanding of the genomic targets of these chromatin modifiers. Here, we review recent developments in basic and translational research that have provided tantalizing clues that may be used to unlock the therapeutic potential of the epigenome in heart failure. Additionally, we provide a hypothesis to explain how signal-induced crosstalk between histone tail modifications and long non-coding RNAs triggers chromatin architectural remodeling and culminates in cardiac hypertrophy and fibrosis.

KEYWORDS:

cardiac hypertrophy; epigenetics; fibrosis; heart failure

PMID:
30416708
PMCID:
PMC6206605
DOI:
10.12688/f1000research.15797.1
[Indexed for MEDLINE]
Free PMC Article

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