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