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.
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