Stress-activated cardiac signaling cascades ultimately converge on defined transcriptional pathways that drive pathologic gene expression programs. Excessive or prolonged activation of these pathways culminates in hypertrophy, fibrosis, and contractile dysfunction....
CITATION STYLE
Anand, P., Munir, A., & Haldar, S. M. (2016). BET Bromodomains and P-TEFb in Cardiac Transcription and Heart Failure Pathogenesis (pp. 283–296). https://doi.org/10.1007/978-3-319-41457-7_12
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