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Demonstrates that BRD4 drives cardiac fibroblast activation via p38 signaling, highlighting BRD4 inhibitors as potential targeted therapies for heart failure.
These findings define BRD4 as a central regulator of the pro-fibrotic cardiac fibroblast phenotype, establish a p38-dependent signaling circuit for epigenetic reprogramming in heart failure, and uncover a novel role for Sertad4. The work provides a mechanistic foundation for the development of BRD4 inhibitors as targeted anti-fibrotic therapies for the heart.
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Stratton et al. (2019) studied this question.
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