The growth response of resident glomerular cells is determined by the under
lying disease. Thus glomerular cells can proliferate, fail to proliferate,
hypertrophy or apoptose. Cell growth is controlled by cell cycle regulatory
proteins, and cell proliferation requires that cyclin-dependent kinases (C
DK) be activated by partner cyclins. Inhibiting CDK2 reduces mesangial cell
proliferation. Mesangial cell proliferation also requires that levels of s
pecific cyclin kinase inhibitors (CKI) decrease. In contrast the visceral g
lomerular epithelial cells' inability to proliferate may be due to increase
d levels of CKI, Moreover it is becoming increasingly clear that mesangial
cell hypertrophy in diabetes requires increased CKI expression. Finally, ap
optosis, which is often linked to proliferation, may also be due to the inc
reased activity of CDK2. Thus, identifying specific cell cycle regulatory p
roteins following injury may provide future targets for therapy in glomerul
ar disease.