Helen Vlassara, MD, Icahn School of Medicine at Mount Sinai

Helen Vlassara, MD
Helen Vlassara, MD

A focus of the Vlassara laboratory is to broaden the working model on pathogenic processes and obtain tools for prevention/intervention treatments of the complications of aging and diabetes. These complex entities reflect multiple interactions of environmental and genetic parameters. Her studies have defined: a) the chemical and cellular-toxicity of advanced glycation; b) a new receptor system that recognizes AGE-modified molecules (AGE-receptor); c) genetic factor(s) influencing the AGE-receptor function. Cellular activation via this receptor contributes to vascular, renal, and neuronal dysfunction under conditions of AGE-overaccumulation, as in aging, diabetes, or renal impairment. These factors, combined with environmental AGEs, eg., diet and tobacco smoke, can contribute to tissue injury, leading to chronic degenerative disorder. Dr. Vlassara's studies have applied a broad range of molecular, cell-culture, and animal-based approaches to confirm a cause-and-effect relationship between AGEs and pathology. Concurrently, they also have produced novel quantitative and sensitive diagnostic methods and highly effective therapies that are actively tested.

The Investigator's Annexe Part of The Investigator's Annexe program.



  1. Cai W, Gao GD, Zhu L, Peppa M, Vlassara H. Oxidative stress-inducing carbonyl compounds from commn foods: novel mediators of cellular dysfunction. Mol Med 8: 337-346, 2002.
  2. Vlassara H, Cai W, Crandall J, Goldberg T, Oberstein R, Dardaine V, Peppa M, Rayfield EJ. Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy Proc Natl Acad Sci USA. 99: 15596-15601, 2002.
  3. Cai W, He JC, Zhu L, Chen X, Zheng F, Striker GE, Vlassara H. Oral glycotoxins determine the effects of calorie restriction on oxidant stress, age-related diseases, and lifespan. Am J Pathol 173: 327-336, 2008.
  4. Torreggiani M, Liu H, Wu J, Zheng F, Cai W, Striker GE, Vlassara H. Advanced glycation end product receptor-1 transgenic mice are resistant to inflammation, oxidant stress, and post-injury intima hyperplasia Am J Pathol 175: 1722-1732, 2009.
  5. Cai W, Ramdas M, Zhu L, Striker GE, Vlassara H. Oral advanced glycation endproducts (AGEs) promote insulin resistance and diabetes by depleting the antioxidant defenses AGE receptor-1 and sirtuin 1. Proc Natl Acad Sci USA 109: 15888-15893, 2012.