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Howard Allan Rockman

Edward S. Orgain Distinguished Professor of Cardiology, in the School of Medicine
Medicine, Cardiology
Duke Box 102151, Durham, NC 27710
226 Clin Res Lab Bldg, Duke Box 102151, Durham, NC 27710

Overview


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.

Current Appointments & Affiliations


Edward S. Orgain Distinguished Professor of Cardiology, in the School of Medicine · 2008 - Present Medicine, Cardiology, Medicine
Professor of Medicine · 2002 - Present Medicine, Cardiology, Medicine
Professor in Cell Biology · 2011 - Present Cell Biology, Basic Science Departments

Recent Publications


Antibodies expand the scope of angiotensin receptor pharmacology.

Journal Article Nat Chem Biol · December 2024 G-protein-coupled receptors (GPCRs) are key regulators of human physiology and are the targets of many small-molecule research compounds and therapeutic drugs. While most of these ligands bind to their target GPCR with high affinity, selectivity is often l ... Full text Link to item Cite

USP20 deletion promotes eccentric cardiac remodeling in response to pressure overload and increases mortality.

Journal Article Am J Physiol Heart Circ Physiol · November 1, 2024 Left ventricular hypertrophy (LVH) caused by chronic pressure overload with subsequent pathological remodeling is a major cardiovascular risk factor for heart failure and mortality. The role of deubiquitinases in LVH has not been well characterized. To def ... Full text Link to item Cite
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Recent Grants


Stimulating Access to Research in Residency (StARR) - NHLBI

Inst. Training Prgm or CMEPreceptor · Awarded by National Heart, Lung, and Blood Institute · 2018 - 2028

Mechanisms of Maladaptation in Heart Failure

ResearchPrincipal Investigator · Awarded by National Heart, Lung, and Blood Institute · 1996 - 2027

Building Interdisciplinary Research Careers in Women's Health - BIRCWH

Inst. Training Prgm or CMEMentor · Awarded by National Institutes of Health · 2002 - 2027

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Education, Training & Certifications


McGill University (Canada) · 1983 M.D.