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Laboratory of Changli Wei, MD, PhD

Changli Wei, MD, PhD embarked on renal research in 2002, studying the molecular mechanisms of nephrotic syndrome, a group of kidney disease that are seemingly mild but often lead to chronic kidney failure. Since 2004, Wei has been largely focusing on urokinase receptor (uPAR) and its different sub-forms. Together with Jochen Reiser, MD, PhD, Wei and colleagues have defined the uPAR-v3 integrin signaling pathway in regulating podocyte foot process structure and function. The fact that uPAR has its soluble forms (suPAR) has prompted Wei and Reiser to identify its role in focal seqmental glomerulosclerosis (FSGS), for which a circulating permeability factor has long been thought responsible, but searching for such factors has been proved a holy grill. With a series of animal models and several large cohorts of FSGS patients, the team’s work strongly suggests that suPAR is one of such circulating factors contributing to the pathogenesis of FSGS. This discovery has been hailed a breakthrough in renal research.

Since then, Wei has been continuously driven by the complexity of suPAR, an increasingly fascinating molecule. His current work is to understand the role of different suPAR sub-forms in different disease settings.

Lab location

Wei’s lab is located at the Cohn Research Building, seventh floor.


Wei’s lab is currently funded by National Institutes of Health, Therumo BCT. He receives intramural support as well.


Wei is the author of more than 50 scientific articles.

Selected Publications

  1. Wei C, Lee KH, Khoo HE, Hon WM. Expression of haem oxygenase in cirrhotic rat liver. J Pathol 2003; 199(3):324-34.
  2. Wei C, Cheung W, Heng CK, Gong WK, Chong SS, Yap HK. Interleukin-13 genetic polymorphisms in Singapore Chinese children correlate with long-term outcome of minimal change disease. Nephrol Dial Transplant 2005; 20:728-34
  3. Moller CC, Wei C, Altintas MM, Li J, Ohse T, Pippin JW, Rastaldi MP, Schiavi S, Wawersik S, Kretzler M, Shankland SJ and Reiser J. Induction of TRPC6 channel in acquired forms of proteinuric kidney disease. J Am Soc Nephrol 2007; 18:29-36
  4. Lai KW, Wei C, Tan LK, Tan PH, Chiang GS, Lee CG, Jordan SC and Yap HK. Overexpression of interleukin-13 induces minimal-chang-like nephropathy in rats. J Am Soc Nephrol 2007; 18:1476-1485
  5. Wei C, Möller CC, Altintas MM, Li J, Schwarz K, Zacchigna S, Xie L, Henger A, Schmid H, Rastaldi MP, Cowan P, Kretzler M, Parrilla R, Bendayan M, Gupta V, Nikolic B, Kalluri R, Carmeliet P, Mundel P, and Reiser J. Modification of kidney barrier function by the urokinase receptor. Nature Medicine 2008; 14:55-63
  6. Wei C, El Hindi S, Li J, Fornoni A, Goes N, Sageshima J, Maiguel D, Karumanchi SA, Yap H-K, Saleem M, Zhang Q, Nikolic B, Chaudhuri A, Daftarian P, Salido E, Torres A, Salifu M, Sarwal MM, Schaefer F, Morath C, Schwenger V, Zeier M, Gupta V, Roth D, Rastaldi MP, Burke G, Ruiz P, and Reiser J. Circulating urokinase receptor as cause for focal segmental glomerulosclerosis. Nature Medicine 2011;17:952-60. Cover article
  7. Wei C, Trachtman H, Li J, Dong C, Friedman AL, Gassman JJ, McMahan JL, Radeva M, Heil KM, Trautmann A, Anarat A, Emre S, Ghiggeri GM, Ozaltin F, Haffner D, Gipson DS, Kaskel F, Fischer DC, Schaefer F, Reiser J; PodoNet and FSGS CT Study Consortia. Circulating suPAR in two cohorts of primary FSGS. J Am Soc Nephrol 2012 Dec;23(12):2051-9
  8. Alachkar N, Wei C, Arend LJ, Jackson AM, Racusen LC, Fornoni A, Burke G, Rabb H, Kakkad K, Reiser J, Estrella MM. Podocyte effacement closely links to suPAR levels at time of posttransplantation focal segmental glomerulosclerosis occurrence and improves with therapy. Transplantation. 2013;96(7):649-56.
  9. Delville M, Sigdel TK, Wei C*, Li J, Hsieh SC, Fornoni A, Burke GW, Bruneval P, Naesens M, Jackson A, Alachkar N, Canaud G, Legendre C, Anglicheau D, Reiser J, Sarwal MM. A circulating antibody panel for pretransplant prediction of FSGS recurrence after kidney transplantation. Science Translational Medicine. 2014 Oct 1;6(256):256ra136. * co-first author