Abstract
Cardiovascular disease (CVD) is the biggest cause of mortality and morbidity worldwide, with 80% of the deaths from CVD due to myocardial infarction. Extensive cellular, tissue, and organ remodeling occurs through CVD initiation and progression, which is mediated by stable alterations in gene expression. Covalent modifications on histone proteins regulate chromatin structure and change the accessibility of gene promoter and enhancer regions to transcriptional factors. In this manner, histone modifications and modifiers act to dynamically tune transcription. Histone methylation is generally repressive, whereas acetylation promotes gene expression but the effect of each histone modification is highly context-specific. Dynamic changes in histone modification profiles have been described in cardi0myocyte hypertrophy, heart failure, and vascular disease, with experimental studies revealing these changes as necessary for the initiation or development of CVD. Moreover, preventing these disease-associated changes to histone marks, by modulating histone modifiers, can attenuate or aggravate the CVD phenotype.
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