Apoptosis in glomerulonephritis

Abstract

Although glomerular cell apoptosis may be detrimental in acute and chronic inflammation, it is also a key component of the reparative glomerular remodelling that can follow injury. All glomerular cells are vulnerable to apoptosis although there are often differences in the nature of the initiating stimulus and the factors that are protective. The purpose of this review is to outline how modulation of this process may inhibit glomerular injury and promote tissue repair. In-vitro studies are providing more information on the factors that regulate apoptosis in individual glomerular cell types. It has now become apparent that growth factors such as vascular endothelial growth factor may have protective actions on several cell types and this may facilitate future treatments that promote the survival of multiple cell types within injured glomeruli. Work in this field has also emphasized that many current treatment strategies may exert a beneficial impact upon renal cell death. Although the advent of various antiapoptotic agents such as caspase inhibitors and recombinant growth factors does provide future opportunities to modulate apoptosis for therapeutic gain in patients with glomerulonephritis, there is still some way to go before such reagents are used to treat human disease. However, there is scope for optimism that such treatments will reach the clinic in due course.