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

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 po...

Full description

Saved in:

Bibliographic Details
Published in:	Nephrology, dialysis, transplantation Vol. 18; no. suppl-6; pp. vi8 - vi13
Main Authors:	Griffin, Siân V., Petermann, Arndt T., Durvasula, Raghu V., Shankland, Stuart J.
Format:	Journal Article Conference Proceeding
Language:	English
Published:	Oxford Oxford University Press 01-08-2003
Subjects:	Biological and medical sciences cell cycle Cell Cycle - physiology Cell Cycle Proteins - physiology Cell Differentiation - physiology cyclin Epithelial Cells - physiology glomerular epithelial cell Glomerulonephritis Glomerulosclerosis, Focal Segmental - physiopathology Humans kidney Kidney Glomerulus - physiopathology Medical sciences Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure podocyte proliferation Kidney disease Human Glomerulonephritis Cell culture Urinary system disease cyclin Pathophysiology cell cycle Exploration Kidney Podocyte podocyte proliferation glomerular epithelial cell Epithelial cell
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Description
Summary:	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.
Bibliography:	istex:C59C2E9A6EFD6FF6858F82D8D669A597A5FEC3EA local:gfg1069 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@u.washington.edu ark:/67375/HXZ-1QHB3M4T-M ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1
ISSN:	0931-0509 1460-2385 1460-2385
DOI:	10.1093/ndt/gfg1069