Babak Razani, MD, PhD

Instructor in Medicine

Dr. Razani’s current profile can be found with Cardiovascular Division, Department of Medicine, at Washington University in St. Louis.

Biography

2005-2009 Washington University School of Medicine / Barnes-Jewish Hospital Fellowship in cardiology

2005-2007 Cardiovascular Clinical Fellow

2007-2009 Laboratory of Dr. Clay Semenkovich, Division of Endocrinology, Metabolism, and Lipid Research

2003 – 2005 Washington University School of Medicine / Barnes-Jewish Hospital, Residency in Internal Medicine Physician Scientist Training Program

1996 – 2003 Albert Einstein College of Medicine, Medical Scientist Training Program (M.D., Ph.D.)
M.D. (June 2003)

Ph.D., Molecular Pharmacology (November 2001)
Dissertation with Dr. Michael P. Lisanti
Thesis Title: Insights Into Caveolae, The Caveolins, and The Signaling Hypothesis: A biochemical, Cellular and Genetic Approach

1992 – 1996 University of California at Berkeley
B.S., Electrical Engineering and Computer Science
B.A., Molecular and Cellular Biology

Research Interests

I am currently involved in several projects in the field of cardiovascular biology in the laboratory of Dr. Clay Semenkovich. Recently, our laboratory has discovered that absence of Ataxia-Telangiectasia Mutated (ATM) (a protein traditionally thought to be involved in DNA damage repair and cancer biology) leads to atherosclerotic progression in mouse models. Furthermore, Chloroquine (the traditional treatment modality for malaria) was found to be an activator of ATM signaling and thus play a protective role in insulin resistance and atherosclerosis. We are now further characterizing the underlying mechanisms involved in these initial observations; specifically, we are focusing on ATM’s and chloroquine’s roles in macrophage inflammatory signaling and contribution to atherosclerosis. (2) In a second project, we have been generating mice with selective ablation of fatty acid synthase (FAS) in the myocradium in order to study the effects of aberrant fatty acid metabolism in heart function. In the past few years, several lines of evidence link FAS with PPARalpha function. Thus, the effects of these genetic manipulations on PPARalpha signaling and fatty acid oxidation will be a major initial focus of this project.

PubMed