William E. Mitch, M.D., F.A.S.N., F.A.H.A.
Professor and Chair
Department of Medicine - Nephrology
- M.D., Harvard Medical School, Boston, MA
- Residency, Brigham and Women's Hospital, Boston, MA
- Resident Fellow, Johns Hopkins Hospital, Baltimore, MD
- Control of protein metabolism in catabolic conditions
- Treatment of patients with chronic renal disease and methods for delaying loss of kidney function
- Hu Z, Lee IH, Wang X, Sheng H, Zhang L, Du J, Mitch WE. PTEN expression contributes to the regulation of muscle protein degradation in diabetes. Diabetes. 2007. 56(10):2449-56.
- Bailey JL, Price SR, Zheng B, Hu Z, Mitch WE. Chronic kidney disease causes defects in signaling through the insulin receptor substrate/phosphatidylinositol 3-kinase/Akt pathway: implications for muscle atrophy. J Am Soc Nephrol. 2006. 17:1388-94.
- Wang X, Hu J, Hu Z, Du J, Mitch WE. Insulin resistance accelerates muscle protein degradation: activation of the ubiquitin-proteasome pathway by defects in muscle cell signaling. Endocrinology. 2006. 147:4160-8.
- Workeneh BT, Rondon-Berrios H, Zhang L, Hu Z, Ayehu G, Ferrando A, Wang H, Storer T, Kopple JD, Du J, Mitch WE. Development of a diagnostic method for detecting increased muscle protein degradation in patients with catabolic conditions J Am Soc Nephrol. 2006. 17:3233-9.
- Mitch WE. Cachexia in chronic kidney disease: a link to defective central nervous system control of appetite. J Clin Invest. 2005. 115:1476-8.
- Song Y-H, Li, Du J, Mitch WE, Rosenthal N, Delafontaine P. Muscle-specific expression of insulin-like growth factor-1 blocks angiotensin II-induced skeletal muscle wasting. J Clin Invest. 2005. 115:451-8.
- Du J, Wang X, Miereles C, Bailey JL, Debigare R, Zheng B, Price SR, Mitch WE. Activation of caspase 3 is an initial step triggering accelerated muscle proteolysis in catabolic conditions. J Clin Invest. 2004. 113:115-23.