Howard Allan Rockman, MD

Professor of Medicine
Edward S. Orgain 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, Durham, NC 27710
Phone (919) 668-2520
Email address h.rockman@duke.edu

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

Publications

Rockman, HA. "Tempus fugit." J Clin Invest 123, no. 3 (March 1, 2013): 935-936.

PMID
23454753
Full Text

Tang, H, Xiao, K, Mao, L, Rockman, HA, and Marchuk, DA. "Overexpression of TNNI3K, a cardiac-specific MAPKKK, promotes cardiac dysfunction." J Mol Cell Cardiol 54 (January 2013): 101-111.

PMID
23085512
Full Text

Tang, H, Xiao, K, Mao, L, Rockman, HA, and Marchuk, DA. "Overexpression of TNNI3K, a cardiac-specific MAPKKK, promotes cardiac dysfunction." Journal of Molecular and Cellular Cardiology 54, no. 1 (2013): 101-111.

Full Text

Perrino, C, and Rockman, HA. "Modulating G protein-coupled receptors to effect reverse cardiac remodeling." In Cardiac Remodeling: Molecular Mechanisms, 159-177. January 1, 2013.

Full Text

Rockman, HA. "Clinical medicine." JOURNAL OF CLINICAL INVESTIGATION 122, no. 12 (December 2012): 4303-4303.

Full Text

Kim, K-S, Abraham, D, Williams, B, Violin, JD, Mao, L, and Rockman, HA. "β-Arrestin-biased AT1R stimulation promotes cell survival during acute cardiac injury." Am J Physiol Heart Circ Physiol 303, no. 8 (October 15, 2012): H1001-H1010.

PMID
22886417
Full Text

Lee, C-L, Moding, EJ, Cuneo, KC, Li, Y, Sullivan, JM, Mao, L, Washington, I, Jeffords, LB, Rodrigues, RC, Ma, Y, Das, S, Kontos, CD, Kim, Y, Rockman, HA, and Kirsch, DG. "p53 functions in endothelial cells to prevent radiation-induced myocardial injury in mice." Science signaling 5, no. 234 (July 24, 2012): ra52-.

PMID
22827996
Full Text

Houser, SR, Margulies, KB, Murphy, AM, Spinale, FG, Francis, GS, Prabhu, SD, Rockman, HA, Kass, DA, Molkentin, JD, Sussman, MA, Koch, WJ, American Heart Association Council on Basic Cardiovascular Sciences, Council on Clinical Cardiology, and and Council on Functional Genomics and Translational Biology, . "Animal models of heart failure: a scientific statement from the American Heart Association." Circ Res 111, no. 1 (June 22, 2012): 131-150. (Review)

PMID
22595296
Full Text

Rockman, HA. "Great expectations." J Clin Invest 122, no. 4 (April 2012): 1133-.

PMID
22466653
Full Text

Casad, ME, Yu, L, Daniels, JP, Wolf, MJ, and Rockman, HA. "Deletion of Siah-interacting protein gene in Drosophila causes cardiomyopathy." Mol Genet Genomics 287, no. 4 (April 2012): 351-360.

PMID
22398840
Full Text

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