Professor Emeritus, Department of Internal Medicine
Division of Nephrology, University of Michigan Medical Center
Dr. Roger Wiggins is a Professor Emeritus in the Department of Internal Medicine at the University of Michigan. His lab is credited with identifying and cloning particular podocyte proteins that can be used as markers for understanding podoctyte biology. The lab is currently constructing several transgenic mouse models to explore the importance of podocyte number.
Dr. Wiggins received his M.B. and B.Chir. degrees from Cambridge University in England. He completed his residency at London Teaching Hospitals, focusing on nephrology, neurology and cardiology. Dr. Wiggins completed his fellowship in immunopathology at the Scripps Clinic and Research Foundation in La Jolla, California.
Venkatareddy M, Wang SQ, Yang Y, Patel S, Wickman L, Nishizono R, Chowdhury M, Hodgin J, Wiggins PA and Wiggins RC. Estimating podocyte number and density in histologic sections. J Am Soc Nephrol. 2014.
Wickman L, Afshinnia F, Yang Y, Wang SQ, Wang F, Chowdhury M ,Graham D, Hawkins J, Nishizono R, Tanzer M, Wiggins J ,Escobar GA, Rovin B , Song P, Gipson D, Kershaw D, Wiggins RC. Urine podocyte mRNAs, proteinuria and progression in human glomerular diseases. J Am Soc Nephrol. 2013; 24:2081-95.
Ashraf S, Gee HY,1 Woerner S, XieLX, Vega-Warner V,Lovric S, Fang H, Song X, Cattran DC, Avila-Casado C, Paterson AD, Nitschké P, Bole-Feysot C, Cochat P, Esteve-Rudd J, Haberberger B, Allen SJ, Zhou W, Airik R, Otto E, Barua M, Al-Hamed MH, Kari JK, Evans J, Bierzynska A, Saleem MA, Böckenhauer D, Kleta R, El DesokyS, Hacihamdioglu DO, Gok F, Washburn J, Wiggins RC, Choi M, Lifton R, Levy S, Han Z,Salviati S, Prokisch H, Williams DS, Pollak M, Clarke CF, Pei Y, Antignac C, and Hildebrandt F. ADCK4 mutations promote steroid-resistant nephrotic syndrome through CoQ10 biosynthesis disruption. J Clin Invest. 2013; 123:5179-89.
Gee, HY, Ashraf S, Saisawat P, Hurd TW Vega-Warner V, Fang H, Beck B, Gribouval O, Zhou W, Diaz K, Natarajan S, Wiggins RC, Lovric S, Chernin G, Schoeb DS, Ovunc B, Frishberg Y, Soliman NA, Fathy HM, Goebel H, Hoefele J, Weber LT, Innis JW, Faul C, Washburn Antignac JC, Levy S, Otto EA, and Hildebrandt F. ARHGDIA mutations cause nephrotic syndrome by defective RHO GTPase signaling. J Clin Invest. 2013; 123:3243-53.
Fukuda A, Chowdhury M, Venkatareddy M, Wang SQ, Nishizono R, Wickman L, Wiggins J, Muchayi T, Fingar D, Shedden K, Inoki K and Wiggins RC. Growth-dependent podocyte failure causes glomerulosclerosis. J Am Soc Nephrol. 2012; 23:1351-63.
Inoki K, Mori H, Wang J, Suzuki T, Hong SK, Yoshida S, Blattner , Ikenoue T, Rüegg M, Hall M, Kwiatkowski D, Rastaldi M, Huber T, Kretzler M, Holzman L, Wiggins RC, Guan K-L. mTORC1 activation in podocytes is a critical step in the development of diabetic nephropathy J Clin Invest. 2011; 121: 2181-96.
Fukuda A, Wickman LT, Venkatareddy M, Sato Y, Chowdhury M, Wang SQ, Shedden K, Dysko R, Wiggins J and Wiggins RC. Progression is caused by angiotensin II-dependent persistent podocyte loss from destabilized glomeruli. Kidney Int. 2011; 81:40-55.