Division of Endocrinology & Diabetes

Michael A. Brownlee, M.D.

Dr. Michael A. Brownlee

Professor, Department of Medicine (Endocrinology)

Professor, Department of Pathology

Anita and Jack Saltz Chair in Diabetes Research


Selected Publications

  1. D'Apolito M, Du X, Zong H, Catucci A, Maiuri L, Trivisano T, Pettoello-Mantovani M, Campanozzi A, Raia V, Pessin JE, Brownlee M, Giardino I (2010). Urea-induced ROS generation causes insulin resistance in mice with chronic renal failure. J Clin Invest. 4;120(1):203-13.
  2. Yao D, Brownlee M. (2010) Hyperglycemia-induced reactive oxygen species increase expression of the receptor for advanced glycation end products (RAGE) and RAGE ligands. Diabetes. 59(1):249-55.
  3. Bierhaus A, Fleming T, Stoyanov S, et al. (2012) Methylglyoxal modification of Na(v)1.8 facilitates nociceptive neuron firing and causes hyperalgesia in diabetic neuropathy. Nat Med. 18(9):1445
  4. Giacco, F., Du, X., D’Agati, V.D., Milne, R., Sui, G., Geoffrion, M., and Brownlee, M (2014). Knockdown of Glo1 mimics diabetic nephropathy in non-diabetic mice. Diabetes. 63(1):291-9.5.
  5. Giacco, F., Du, X., Carratu, A., Gerfen, G.J., D’Apolito, M., Giardino, I., Rasola, A., Marin, O., Divakaruni, A.S., Murphy, A.N., Shah, M.S., and Brownlee, M. (2015). GLP-1 cleavage product reverses persistent ROS generation after transient hyperglycemia by disrupting an ROS-generating feedback loop. Diabetes 64: (in press).

Material in this section is provided by individual faculty members who are solely responsible for its accuracy and content.


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Bronx, NY 10461

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