Readers, Writers, and Erasers: Chromatin as the Whiteboard of Heart Disease

• Published in: Circulation research Vol. 116; no. 7; pp. 1245 - 1253
• Main Authors: Gillette, Thomas G., Hill, Joseph A.
• Format: Journal Article
• Language: English
• Published: United States American Heart Association, Inc 27.03.2015
• Subjects: Acetylation; Animals; Cardiomegaly - genetics; Cardiomegaly - metabolism; Cardiotonic Agents - therapeutic use; Chromatin - genetics; Chromatin - metabolism; Chromatin - ultrastructure; Chromatin Assembly and Disassembly; Epigenesis, Genetic; Fetal Heart - growth & development; Gene Expression Regulation; Heart - embryology; Heart Diseases - genetics; Histone Acetyltransferases - physiology; Histone Deacetylase Inhibitors - therapeutic use; Histone Deacetylases - physiology; Histone Deacetylases - therapeutic use; Histone Demethylases - physiology; Histone-Lysine N-Methyltransferase - physiology; Histones - physiology; Humans; Methylation; Multiprotein Complexes; Myocardial Ischemia - genetics; Myocardial Ischemia - metabolism; Myocardium - metabolism; Nucleosomes - genetics; Nucleosomes - ultrastructure; Protein Processing, Post-Translational; Protein Structure, Tertiary; Rats; Transcription, Genetic; chromatin; chromatin assembly and disassembly; epigenomics
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/CIRCRESAHA.116.303630

Dynamic packaging of DNA into strings of nucleosomes is a major mechanism whereby eukaryotic cells regulate gene expression. Intricate control of nucleosomal structure and assembly governs access of RNA polymerase II to DNA and consequent RNA synthesis. As part of this, post-translational modifications of histone proteins are central to the regulation of chromatin structure, playing vital roles in regulating the activation and repression of gene transcription. In the heart, dynamic homeostasis of histone modification—driven by the actions of modifiers and recruitment of downstream effectors—is a fundamental regulator of the transcriptional reprogramming that occurs in the setting of disease-related stress. Here, we examine the growing evidence for histone modification as a key mechanism governing pathological growth and remodeling of the myocardium.