Purpose of review Heart failure is not simply a pump that has grown tired; it is a tissue that adapts and then, too often, becomes locked into its adaptations. This review examines how epigenetic regulation – chromatin accessibility, histone modifications, DNA methylation and hydroxymethylation, and the reader complexes that interpret these marks – converts transient stress into durable transcriptional programs. We focus on the mechanisms by which the failing heart acquires regulatory “memory,” and on the chromatin control nodes that are emerging as actionable targets for therapy and for biomarker development. Recent findings Three lines of evidence are reshaping the field. First, the failing-heart transcriptome is increasingly governed by a tractable set of chromatin control points: acetylation balance [histone deacetylases (HDACs) versus histone acetyltransferases (HATs) such as p300/CREB-binding protein (CBP)] and acetyl-lysine readers [bromodomain and extraterminal (BET) proteins, including bromodomain-containing protein 4 (BRD4)] that amplify hypertrophic, inf
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