Babak Razani, MD, PhD
Assistant Professor of Medicine
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Education
- B.S., Electrical Engineering and Computer Science: University of California, Berkeley, CA (1996)
- B.A., Molecular and Cellular Biology: University of California, Berkeley, CA (1996)
- Ph.D., Molecular Pharmacology: Albert Einstein College of Medicine, Bronx, NY (2001)
- Medical Scientist Training Program (M.D.-Ph.D.): Albert Einstein College of Medicine, Bronx, NY (2003)
- M.D.: Albert Einstein College of Medicine, Bronx, NY (2003)
- Residency, Internal Medicine: Barnes-Jewish Hospital, Washington University School of Medicine, St. Louis, MO (2005)
- Fellowship, Cardiology: Barnes-Jewish Hospital, Washington University School of Medicine, St. Louis, MO (2009)
Board Certifications
- Cardiovascular Diseases
- Echocardiology
Recognition
1994
Eta Kappa Nu (National Electrical Engineering Honor Society)
Tau Beta Pi (National Engineering Honor Society)
1995
University of California Presidential Undergraduate Fellowship
2002
The Albert Einstein College of Medicine Julius Marmur Research Award (for best Ph.D. dissertation)
2003
Dean’s Commendation Award, Albert Einstein College of Medicine
2008
Pfizer-Washington University Junior Fellow Award
2009
Washington University Cardiovascular Division Burton E. Sobel Award for Excellence in Cardiovascular Research
2010
K08 Career Development Award, National Institutes of Health
2011
Outstanding Young Investigator Award, American Society fo Clinical Investigation / Association of American Physicians Annual Meeting
2012
Barnes-Jewish Hospital / Washington University Internal Medicine Attending of the Month Award – January
2013
Roger Davis Investigator Award for Transitional Faculty , Kern Lipid Conference
2nd Place Finalist, Northwestern Cardiovascular Young Investigators’ Forum
2014
Irvine H. Page Young Investigator Research Award, ATVB Scientific Sessions
2015
David L. Williams Lecture and Scholarship Award, Kern Lipid Conference
Clinical Interests
Clinical Cardiology
Echocardiography
Research Interests
Atherosclerosis is a chronic and insidious process wherein the arterial lining is compromised by lipid and cellular infiltration. Atherosclerotic plaque progression is the underlying cause of the majority of cardiovascular diseases including myocardial infarction and strokes leading to tremendous morbidity and mortality worldwide. Understanding the pathophysiology of plaque formation and progression remains an important area of investigation both scientifically and clinically, serving as the basis for future therapeutics. Inflammatory cells, especially macrophages, play a central role in atherosclerosis. Elucidation of cellular processes that are affected in plaque macrophages has led to our understanding that among other things, aberrant lipid homeostasis and inflammation are critical to plaque progression.
Recent work on autophagy, or the process by which cells turn over long-lived organelles and proteins, has revealed that atherosclerotic macrophages manifest features of autophagy deficiency and that this deficiency is likely pathogenic as mice with selective disruption of macrophage autophagy (ATG5-null) are pro-inflammatory, have defects in lipid handling, and develop large and complex atherosclerotic lesions (Razani B, et al Cell Metab 2012; Liao X, et al Cell Metab 2012). Although the exact mechanisms of autophagy deficiency and its downstream sequelae are currently unknown, our preliminary data suggests that disruptions of autophagosome processing through lysosomes and progressive lysosomal dysfunction likely play important roles. The following projects in the lab are focused on studying the autophagolysosomal system in atherosclerosis:
1) Determining the degree of lysosomal dysfunction in Plaque Macrophages and its effect on atherogenesis
2) Investigating the potential for enhanced autophagy/lysosomal pathways to ameliorate macrophage dysfunction and atherosclerosis
3) Evaluating the pathogenic role of Inclusion Body formation in Atherosclerosis