These findings establish that pharmacologically targeting innate inflammatory and profibrotic myocardial signaling networks at the level of chromatin is effective in animal models and human cardiomyocytes, providing the critical rationale for further development of BET inhibitors and other epigenomic medicines for HF.
Here, we review the current understanding of chromatin-dependent signal transduction in cardiac gene control, and highlight the potential for pharmacologic regulation of BET acetyl-lysine binding proteins as a means of treating heart failure.
This study implicates epigenetic readers as essential effectors of transcriptional pause release during HF pathogenesis and identifies BET coactivator proteins as therapeutic targets in the heart.