Chemical modifications to nucleosomal DNA and histone tails greatly influence transcription of adjacent and distant genes, a mode of gene regulation referred to as epigenetic control. Here, the authors summarize recent findings that have illustrated crucial roles for epigenetic regulatory enzymes and reader proteins in the control of cardiac fibrosis. Particular emphasis is placed on epigenetic regulation of stress-induced inflammation and fibroblast activation in the heart. The potential of developing innovative small molecule "epigenetic therapies" to combat cardiac fibrosis is highlighted.
Keywords: Ang II, angiotensin II; BET, bromodomain and extraterminal protein; DNMT, DNA methyltransferase; ECM, extracellular matrix; HAT, histone acetyltransferase; HDAC, histone deacetylase; IL, interleukin; KDM, lysine demethylase; KMT, lysine methyltransferase; LPS, lipopolysaccharide; MI, myocardial infarction; NF-κB, nuclear factor-κB; SASP, senescent-associated secretory phenotype; SE, super-enhancer; SMA, smooth muscle actin; TET, ten-eleven translocation; TNF, tumor necrosis factor; TSA, trichostatin A; Treg, regulatory T cell; VPA, valproic acid; epigenetics; fibroblast; fibrosis; inflammation.