Renal tubulointerstitial fibrosis. New thoughts on its development and progression.
Current investigation of the pathogenesis of tubulointerstitial injury indicates that both interstitial fibroblasts and renal tubular epithelial cells promote extracellular matrix accumulation. Moreover, two peptides--TGF-beta and angiotensin II--produced locally or delivered in the circulation, appear to play a central role in renal fibrosis. Pharmacologic amelioration of renal fibrosis may require methods directed at multiple factors involved in the fibrotic process, including angiotensin II, TGF-beta, and the proliferation and activation of interstitial fibroblasts.
O'Donnell
M P
MP
Department of Medicine, Hennepin County Medical Center, Minneapolis, USA. mod19@mail.idt.net
D000804:Angiotensin II / Q000378:metabolism; D004848:Epithelium / Q000502:physiology; D005355:Fibrosis; D006801:Humans; D007676:Kidney Failure, Chronic / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology*; D007684:Kidney Tubules / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D016212:Transforming Growth Factor beta / Q000502:physiology
D016212:Transforming Growth Factor beta; D000804:Angiotensin II