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Nephrol Dial Transplant (2003) 18: VI8-VI13
© 2003 European Renal Association-European Dialysis and Transplant Association

Podocyte proliferation and differentiation in glomerular disease: role of cell-cycle regulatory proteins

Siân V. Griffin, Arndt T. Petermann, Raghu V. Durvasula and Stuart J. Shankland

Division of Nephrology, University of Washington Medical Center, Seattle, WA, USA

Correspondence and offprint requests to: Stuart J. Shankland MD, Director, Nephrology Fellowship Program, Division of Nephrology, University of Washington Medical Center, Box 356521, Seattle, WA 98195, USA. Email: stuartjs{at}u.washington.edu

Abstract

Injury to the podocyte underlies many forms of glomerular disease. In contrast to mesangial and endothelial cells, podocytes do not typically proliferate. Moreover, the lack of proliferation is thought to underlie the development of glomerulosclerosis. Studies have recently shown that the lack of podocyte proliferation is due to an increase in cyclin-dependent kinase inhibitors, which arrest the cell cycle. Current work is aimed at further delineating the mechanisms regulating podocyte proliferation.

Keywords: cell cycle; cyclin; glomerular epithelial cell; kidney; podocyte proliferation


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