Howard Allan Rockman, MD

Professor of Medicine
Edward S. Orgain Distinguished Professor of Cardiology, in the School of Medicine
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 genes ablated 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.

Education and Training

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


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.” Nature Communications 8, no. 1 (November 22, 2017): 1706.

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Gareri, Clarice, Joao A. Paulo, Alem W. Kashai, Jialu Wang, Kenji Hanada, Dean P. Staus, Laura M. Wingler, Steven P. Gygi, and Howard A. Rockman. “Mechanical Stretch Activates Biased AT1R Signaling Through a Unique B-arrestin Conformation.” In Circulation, Vol. 136. LIPPINCOTT WILLIAMS & WILKINS, 2017.


Jean-Charles, Pierre-Yves, Samuel Mon-Wei Yu, Dennis Abraham, Reddy Peera Kommaddi, Lan Mao, Ryan T. Strachan, Zhu-Shan Zhang, et al. “Mdm2 regulates cardiac contractility by inhibiting GRK2-mediated desensitization of β-adrenergic receptor signaling.” Jci Insight 2, no. 17 (September 7, 2017).

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Abraham, Dennis M., Robert T. Davis, Chad M. Warren, Lan Mao, Beata M. Wolska, R John Solaro, and Howard A. Rockman. “β-Arrestin mediates the Frank-Starling mechanism of cardiac contractility.” Proc Natl Acad Sci U S A 113, no. 50 (December 13, 2016): 14426–31.

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Jean-Charles, Pierre-Yves, Samuel Mon-Wei Yu, Lan Mao, Reddy Perra Kommadi, Zhushan Zhang, Jonathan Stiber, Dawn Bowles, et al. “Beta(1)-Adrenergic Receptor-induced Cardiac Contractility is dependent on MDM2-mediated GRK2 Turnover.” In Circulation Research, 119:E162–63. LIPPINCOTT WILLIAMS & WILKINS, 2016.