Role of apoptosis in renal injury

Nephrologists are now investigating the involvement of apoptosis, or programmed cell death, in various renal diseases. Evidence suggests that abnormalities of apoptosis may contribute to the development of glomerular and tubular diseases. In tissue remodeling after glomerular injuries, excess apoptosis may be associated with cell deletion of glomerular sclerosis. Increased apoptosis may mediate the resolution of glomerular hypercellularity in experimental mesangial proliferation. Reactive oxygen species, deprivation of growth factors, anti-Thy 1 monoclonal antibodies and anti-Fas antibodies are capable of inducing apoptosis in cultured mesangial cells. In renal tubular diseases, apoptosis may be associated with tubular atrophy after ureteral obstruction, tubular damage after ischemia-reperfusion or toxic drugs, and the development of polycystic kidney disease. Infiltrative leukocytes in the glomerulus and renal interstitium undergo apoptosis during inflammation. Thus, apoptosis appears to play a significant role in many renal diseases, and we should consider the regulation of apoptosis in the treatment of these disorders.