Tubular deficiency of von Hippel-Lindau attenuates renal disease progression in anti-GBM glomerulonephritis.

ABSTRACT: In many kidney diseases, the original insult primarily involves the glomerulus and may then pass onto the tubulointerstitium. Several hypotheses link glomerular disease to tubular injury; perhaps the foremost hypothesis involves chronic tubular hypoxia. The reported effects of hypoxia and consecutive stabilization of hypoxia-inducible factors (HIFs), however, are controversial. Hypoxia induces interstitial fibrosis but also has beneficial effects on renal disease progression when HIF is activated pharmacologically. To analyze the impact of HIF on tubulointerstitial disease development in primary glomerular disease, transgenic von Hippel Lindau (VHL)-knockout mice were generated and null expression was induced before the onset of autoimmune IgG-mediated anti-glomerular basement membrane glo

SUBMITTER: Theilig F 

PROVIDER: S-EPMC3204192 | biostudies-literature | 2011 Nov

REPOSITORIES: biostudies-literature