Epigenetic signatures in cardiac fibrosis, special emphasis on DNA methylation and histone modification

Heart Fail Rev. 2018 Sep;23(5):789-799. doi: 10.1007/s10741-018-9694-z.

Abstract

Cardiac fibrosis is defined as excess deposition of extracellular matrix (ECM), resulting in tissue scarring and organ dysfunction. In recent years, despite the underlying mechanisms of cardiac fibrosis are still unknown, numerous studies suggest that epigenetic regulation of cardiac fibrosis. Cardiac fibrosis is regulated by a myriad of factors that converge on the transcription of genes encoding extracellular matrix protein, a process the epigenetic machinery plays a pivotal role. Epigenetic modifications contain three main processes: DNA methylation, histone modifications, and noncoding RNAs. Here, we review recent studies that have illustrated key roles for epigenetic events in the control of pro-fibrotic gene expression, and highlight the potential of molecule mechanisms that target epigenetic regulators as a means of treating cardiac fibrosis.

Keywords: Cardiac fibrosis; DNA methylation; Epigenetic; Histone modification; Noncoding RNA.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cardiomyopathies / genetics*
  • Cardiomyopathies / metabolism
  • DNA Methylation
  • Epigenesis, Genetic*
  • Extracellular Matrix / metabolism*
  • Fibrosis / genetics
  • Fibrosis / metabolism
  • Histone Code
  • Humans
  • MicroRNAs / genetics
  • Myocardium / metabolism*
  • Protein Processing, Post-Translational / genetics*

Substances

  • MicroRNAs