Physician Profile
Howard Rockman, MD
Education:
Medical School:
McGill University, Montreal, Canada, MD, 1983
Residency:
Montreal General Hospital, McGill University, Canada, Internal Medicine, 1984-1987
Fellowship:
University of California at San Diego, Cardiology, 1987-1989
University of California at San Diego, Cardiology Research, 1989-1991
Clinical Interests/Specialties:
Dr. Rockman has an active research program studying the molecular mechanisms of heart failure. He is also actively involved in teaching cardiovascular pathophysiology for the first-year curriculum in the School of Medicine. In 1991, Dr. Rockman was appointed to the faculty in the Department of Medicine at University of California, San Diego. He joined the faculty at Duke University Medical Center in 1999 and currently holds the position of Associate Professor of Medicine and Cell Biology, and Molecular Genetics. He also serves as the Director of the Cardiology Research Fellowship Program.
Research:
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
- Signaling: G protein-coupled receptor signaling in hypertrophy and heart failure focusing on the interaction of phosphoinositide-3 kinase with b-adrenergic receptors.
- Identification of Strain Specific Modifiers: Quantitative trait loci mapping of gene modifiers that alter the heart failure phenotype using disease-sensitized mouse models.
- 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.
- N-ethyl-N-nitrosourea (ENU) mutagenesis program: To detect mutations in genes previously unrecognized to affect cardiac hypertrophy and heart failure. Chemical mutagenesis is used to create new mouse strains that can then be bred into disease-sensitized mouse models to map disease susceptibility genes.
Hospital Affiliations:
Duke University Medical Center
