Research ArticleHeart Failure

BET bromodomain inhibition suppresses innate inflammatory and profibrotic transcriptional networks in heart failure

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Science Translational Medicine  17 May 2017:
Vol. 9, Issue 390, eaah5084
DOI: 10.1126/scitranslmed.aah5084

Article Information

vol. 9 no. 390

PubMed: 
Print ISSN: 
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History: 
  • Received for publication July 13, 2016
  • Resubmitted January 18, 2017
  • Accepted for publication March 30, 2017
  • .

Author Information

  1. Qiming Duan1,*,
  2. Sarah McMahon1,*,
  3. Priti Anand1,
  4. Hirsh Shah2,
  5. Sean Thomas1,
  6. Hazel T. Salunga1,
  7. Yu Huang1,
  8. Rongli Zhang2,
  9. Aarathi Sahadevan2,
  10. Madeleine E. Lemieux3,
  11. Jonathan D. Brown4,
  12. Deepak Srivastava1,5,
  13. James E. Bradner6,
  14. Timothy A. McKinsey7 and
  15. Saptarsi M. Haldar1,8,
  1. 1Gladstone Institute of Cardiovascular Disease, San Francisco, CA 94158, USA.
  2. 2Institute for Transformative Molecular Medicine and Department of Medicine, Case Western Reserve University School of Medicine and University Hospitals Cleveland Medical Center, Cleveland, OH 44106, USA.
  3. 3BioInfo, Plantagenet, Ontario K0B 1L0, Canada.
  4. 4Division of Cardiovascular Medicine, Department of Medicine, and Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
  5. 5Division of Cardiology, Department of Pediatrics, University of California San Francisco School of Medicine, San Francisco, CA 94158, USA.
  6. 6Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02215, USA.
  7. 7Division of Cardiology, Department of Medicine, Consortium for Fibrosis Research & Translation, University of Colorado, Anschutz Medical Campus, Denver, CO 80204, USA.
  8. 8Division of Cardiology, Department of Medicine, and Cardiovascular Research Institute, University of California San Francisco School of Medicine, San Francisco, CA 94158, USA.
  1. Corresponding author. Email: saptarsi.haldar{at}gladstone.ucsf.edu
  • * These authors contributed equally to this work.

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