Babak Razani, M.D., Ph.D.

Associate Professor
Internal Medicine
Cardiovascular Medicine
Pathology and Immunology

Molecular Cell Biology Program
Immunology Program

  • 362-3688

  • 362-2541

  • 362-0186

  • 823 CSRB-NTA

  • brazani@WUSTL.EDU


  • Atherosclerosis, insulin resistance, obesity, macrophage, autophagy, lysosomal dysfunction, lysosomal biogenesis, inclusion body formation

  • Defining the mechanisms of atherosclerosis, obesity, and diabetes with a focus on the roles of autophagy and lysosomes

Research Abstract:

The Razani laboratory is primarily interested in deciphering the pathogenesis of common metabolic diseases such as Atherosclerosis, Diabetes, Obesity, and Fatty Liver disease.
We particularly focus on macrophages and their behavior in target metabolic tissues that leads to disease progression.
One of the pathways we are very interested in is the autophagy-lysosome system, the primary way cells degrade and process endogenous as well as exogenous cargo.
We have shown that the autophagy-lysosome system becomes dysfunctional at various levels in macrophages and contributes to maladaptive behaviors in metabolic tissues.
Thus, we propose the that if macrophages had an improved degradative capacity by stimulation of their autophagy-lysosome system, one could shift the balance to a more beneficial state and actually take advantage of the macrophages` handling of lipids, cytotoxic protein aggregates, dysfunctional organelles, and inflammatory signaling.
We have developed multiple tools both in vivo and in vitro to mechanistically interrogate many aspects of this paradigm.
These efforts have also led us to develop and characterize several therapeutic strategies that we are in the process of translating to clinical trials.

Areas of interest in the lab include:
Atherosclerotic macrophages
Macrophage polarization
Foam cell formation
Adipose tissue metabolism
Adipose tissue macrophages
Liver metabolism
The autophagy-lysosome system
Lysosomal biogenesis
Lysosomal acidification
Lysosomal acid lipase and lysosomal lipolysis
Selective autophagy (particularly p62/SQSTM1)
mTOR signaling
Differing roles of mTORC1 and mTORC2
Nanoparticle delivery systems
iPSC (induced pluripotent stem cells)

Selected Publications:

Evans TD, Sergin I, Zhang X, and Razani B. (2017) Target Acquired: Selective Autophagy in
Cardiometabolic Disease. Science Signaling. 10: eaag2298.

Sergin I, Bhattacharya S, Emanuel R, Esen E, Stokes CJ, Evans TD, Arif B, Curci JA, and Razani B. (2016) Inclusion bodies enriched for p62 and polyubiquitinated proteins in macrophages protect against atherosclerosis. Science Signaling. 9: ra2.

Evans TD, Sergin I, Zhang X, and Razani B. (2016) Modulating Oxysterol Sensing to Control Macrophage Apoptosis and Atherosclerosis. Circ Res. 119: 1258-1261.

Leng S, Iwanowycz S, Saaoud F, Wang J, Wang Y, Sergin I, Razani B, and Fan D. (2016) Ursolic acid enhances macrophage autophagy and attenuates atherosclerosis. J Lipid Res. 57: 1006-16.

Sergin I, Evans TD, and Razani B. (2015) Degradation and Beyond: The Macrophage Lysosome as a Nexus for Nutrient Sensing and Processing in Atherosclerosis. Curr Opin Lipidol. 26: 394-404.

Emanuel R, Sergin I, Bhattacharya S, Turner J, Epelman S, Settembre C, Diwan A, Ballabio A, and Razani B. (2014) Induction of a Lysosomal Biogenesis Program in Atherosclerotic Macrophages Can Rescue Lipid-Induced Lysosomal Dysfunction and Downstream Sequelae. Arterioscler Thromb Vasc Biol. 34: 1942-52.

Sergin I, Evans TD, Bhattacharya S, and Razani B. (2014) Hypoxia in Plaque Macrophages: A New Danger Signal for Interleukin-1β Activation? Circ Res. 115: 817-820.

Sergin I and Razani B. (2014) Self-eating in the Plaque: What Macrophage Autophagy Reveals About Atherosclerosis. Trends Endocrinol Metab. 25: 225-234.

Razani B, Feng C, Coleman T, Emanuel R, Wen H, Hwang S, Ting JP, Virgin HW, Kastan MB, and Semenkovich CF. (2012) Autophagy links inflammasomes to atherosclerotic progression. Cell Metab. 14: 534-44.

Last Updated: 3/13/2017 12:29:41 PM

Central role for autophagy and lysosomal function in the atherogenic phenotype of foam-cell macrophages
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