Howard Allan Rockman, MD

Professor of Medicine
Edward S. Orgain Distinguished Professor of Cardiology, in the School of Medicine
Professor in Molecular Genetics and Microbiology
Professor in Cell Biology
Campus mail 226 Clin Res Lab Bldg, Duke Box 102151, Durham, NC 27710
Phone (919) 668-2520
Email address

Rockman Lab: Molecular Mechanisms of Hypertrophy and Heart Failure

Overall Research Direction: The major focus of this laboratory is to understand the molecular mechanisms of hypertrophy and heart failure. My laboratory uses a strategy that combines state of the art molecular techniques to generate transgenic and gene targeted mouse models, combined with sophisticated physiologic measures of in vivo cardiac function. In this manner, candidate molecules are either selectively overexpressed in the mouse heart or ablated by homologous recombination, which is followed by an in-depth analysis of the physiological phenotype. To model human cardiac disease, we have created several models of cardiac overload in the mouse using both microsurgical techniques and genetic models of cardiac dysfunction.

Areas of Research
1) Signaling: G protein-coupled receptor signaling in hypertrophy and heart failure focusing on the concept of biased signaling of 7 transmembrane receptors.

2) Molecular physiology: In depth physiological analysis of cardiac function in genetically altered mice to understand the role of G protein-coupled receptor signaling pathways on the development of heart failure in vivo.

3) Deletion screens in Drosophila: To detect novel genes important for cardiac function in the adult fly .

Education and Training

  • Cardiology Fellow, Medicine, University of California at San Diego, 1987 - 1991
  • Medical Resident, Medicine, Montreal General Hospital, 1984 - 1987
  • M.D., McGill University (Canada), 1983


Yu, Samuel Mon-Wei, Pierre-Yves Jean-Charles, Dennis M. Abraham, Suneet Kaur, Clarice Gareri, Lan Mao, Howard A. Rockman, and Sudha K. Shenoy. “The deubiquitinase ubiquitin-specific protease 20 is a positive modulator of myocardial β1-adrenergic receptor expression and signaling..” J Biol Chem 294, no. 7 (February 15, 2019): 2500–2518.

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Kim, Jihee, Chad A. Grotegut, James W. Wisler, Tianyu Li, Lan Mao, Minyong Chen, Wei Chen, Paul B. Rosenberg, Howard A. Rockman, and Robert J. Lefkowitz. “β-arrestin 1 regulates β2-adrenergic receptor-mediated skeletal muscle hypertrophy and contractility..” Skelet Muscle 8, no. 1 (December 27, 2018).

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Abraham, Dennis M., Teresa E. Lee, Lewis J. Watson, Lan Mao, Gurangad Chandok, Hong-Gang Wang, Stephan Frangakis, et al. “The two-pore domain potassium channel TREK-1 mediates cardiac fibrosis and diastolic dysfunction..” J Clin Invest 128, no. 11 (November 1, 2018): 4843–55.

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Luttrell, Louis M., Jialu Wang, Bianca Plouffe, Jeffrey S. Smith, Lama Yamani, Suneet Kaur, Pierre-Yves Jean-Charles, et al. “Manifold roles of β-arrestins in GPCR signaling elucidated with siRNA and CRISPR/Cas9..” Sci Signal 11, no. 549 (September 25, 2018).

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Wang, Jialu, Kenji Hanada, Clarice Gareri, and Howard A. Rockman. “Mechanoactivation of the angiotensin II type 1 receptor induces β-arrestin-biased signaling through Gαi coupling..” J Cell Biochem 119, no. 4 (April 2018): 3586–97.

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Wang, Jialu, Kenji Hanada, Dean P. Staus, Michael A. Makara, Giri Raj Dahal, Qiang Chen, Andrea Ahles, Stefan Engelhardt, and Howard A. Rockman. “Gαi is required for carvedilol-induced β1 adrenergic receptor β-arrestin biased signaling..” Nat Commun 8, no. 1 (November 22, 2017).

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