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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


Cardiomyocyte β-arrestins mediate inflammation and cGAS-STING activation in CVB3 viral myocarditis.

Journal Article Am J Physiol Heart Circ Physiol · January 6, 2026 Viral myocarditis is a major cause of sudden cardiac death and can lead to dilated cardiomyopathy in adults. However, effective treatments remain elusive due to an incomplete understanding of its molecular drivers. Here, we investigate the role of β-arrest ... Full text Link to item Cite

A positive allosteric modulator of the β1AR with antagonist activity for catecholaminergic polymorphic ventricular tachycardia.

Journal Article J Clin Invest · December 15, 2025 Orthosteric beta blockers represent the leading pharmacological intervention for managing heart diseases owing to their ability to competitively antagonize β-adrenergic receptors (βARs). However, their use is often limited by adverse effects such as fatigu ... Full text Link to item Cite

Adrenergic Hypersensitivity Drives Ventricular Arrhythmias Following Loss of Plexin-Mediated Cardiac Innervation.

Journal Article JACC Clin Electrophysiol · September 29, 2025 BACKGROUND: Ventricular arrhythmias (VAs) are a leading cause of death and arise from a combination of cardiac muscle injury and dysfunction of the intramyocardial sympathetic nerves that control cardiac electrophysiology. The adrenergic mechanisms by whic ... Full text Link to item Cite
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Recent Grants


iPediHeart: Interdisciplinary Research Training Program for Pediatric Heart Disease

Inst. Training Prgm or CMEMentor · Awarded by National Institutes of Health · 2025 - 2030

Stimulating Access to Research in Residency (StARR) - NHLBI

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

Persistent Injury Activated EC in Fibrosis

FellowshipCollaborator · Awarded by American Heart Association · 2026 - 2027

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Education, Training & Certifications


McGill University (Canada) · 1983 M.D.