Journal
JOURNAL OF PHYSIOLOGY-LONDON
Volume 598, Issue 14, Pages 3005-3014Publisher
WILEY
DOI: 10.1113/JP276745
Keywords
transcription; chromatin; epigenetics; gene regulation; heart failure; cardiac hypertrophy; fibrosis; cardiovascular biology
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Funding
- NIH HHS [HL127240] Funding Source: Medline
- Tobacco-Related Disease Research Program Postdoctoral Fellowship [578649] Funding Source: Medline
- A.P. Giannini Foundation Career Development Award [P0527061] Funding Source: Medline
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Advances in our understanding of the basic biology and biochemistry of chromatin structure and function at genome scales has led to tremendous growth in the fields of epigenomics and transcriptional biology. While it has long been appreciated that transcriptional pathways are dysregulated in failing hearts, only recently has the idea of disrupting altered transcription by targeting chromatin-associated proteins been explored. Here, we provide a brief overview of efforts to drug transcription in the context of heart failure, focusing on the bromo- and extra-terminal domain (BET) family of chromatin co-activator proteins.
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