Babak Razani, M.D., Ph.D.
Fellow in Cardiology
Cardiovascular Division
Department of Medicine
| Office Location: | 829 K Southwest Tower | |
| Mailing Address: |
660 S. Euclid Ave. Campus Box 8127 St. Louis, MO 63110 |
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| Phone: | (314) 747-8282 | |
| Fax: | (314) 362-7641 | |
| E-mail address: |
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Biography
| 2005 - Present | Washington University School of Medicine / Barnes-Jewish Hospital Fellowship in cardiology | |
| 2005-2007 | Cardiovascular Clinical Fellow | |
| 2007-Present |
Laboratory of Dr. Clay Semenkovich Division of Endocrinology, Metabolism, and Lipid Research |
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| 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) | ||
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Dissertation with Dr. Michael P. Lisanti Thesis Title: Insights Into Caveolae, The Caveolins, and The Signaling Hypothesis: A biochemical, Cellular and Genetic Approach |
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| 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.
Research Mentor
