![Michael A. Brownlee](https://assets.montefioreeinstein.org/profiles/images/7647-michael-brownlee.jpg)
Michael A. Brownlee, M.D.
- Professor Emeritus, Department of Medicine (Endocrinology)
- Professor Emeritus, Department of Pathology
- Anita and Jack Saltz Chair in Diabetes Research Emeritus
Phone
Location
- Albert Einstein College of Medicine Jack and Pearl Resnick Campus 1300 Morris Park Avenue Block 308 Bronx, NY 10461
Research Profiles
Selected Publications
- 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.
- 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.
- 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
- 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.
- 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).