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Babak Razani, MD, PhD

Associate Professor of Medicine



Additional Titles

  • Associate Professor of Pathology and Immunology

Related Links


  • 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



Eta Kappa Nu (National Electrical Engineering Honor Society)
Tau Beta Pi (National Engineering Honor Society)


University of California Presidential Undergraduate Fellowship


The Albert Einstein College of Medicine Julius Marmur Research Award (for best Ph.D. dissertation)


Dean’s Commendation Award, Albert Einstein College of Medicine


Pfizer-Washington University Junior Fellow Award


Washington University Cardiovascular Division Burton E. Sobel Award for Excellence in Cardiovascular Research


K08 Career Development Award, National Institutes of Health


Outstanding Young Investigator Award, American Society fo Clinical Investigation / Association of American Physicians Annual Meeting


Barnes-Jewish Hospital / Washington University Internal Medicine Attending of the Month Award – January


Roger Davis Investigator Award for Transitional Faculty , Kern Lipid Conference
2nd Place Finalist, Northwestern Cardiovascular Young Investigators’ Forum


Irvine H. Page Young Investigator Research Award, ATVB Scientific Sessions


David L. Williams Lecture and Scholarship Award, Kern Lipid Conference


Springer Junior Investigator Award, North America Vascular Biology
Organization (NAVBO)


Clinical Interests

Clinical Cardiology

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


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