Title : Glomerular overproduction of oxygen radicals in Mpv17 gene-inactivated mice causes podocyte foot process flattening and proteinuria: A model of steroid-resistant nephrosis sensitive to radical scavenger therapy.

Pub. Date : 1999 Apr

PMID : 10233845






6 Functional Relationships(s)
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1 Glomerular overproduction of oxygen radicals in Mpv17 gene-inactivated mice causes podocyte foot process flattening and proteinuria: A model of steroid-resistant nephrosis sensitive to radical scavenger therapy. Reactive Oxygen Species MpV17 mitochondrial inner membrane protein Mus musculus
2 Glomerular overproduction of oxygen radicals in Mpv17 gene-inactivated mice causes podocyte foot process flattening and proteinuria: A model of steroid-resistant nephrosis sensitive to radical scavenger therapy. Steroids MpV17 mitochondrial inner membrane protein Mus musculus
3 The development of glomerular disease in Mpv17-/- mice was inhibited by scavengers of oxygen radicals (dithiomethylurea) and lipid peroxidation (probucol), but not by steroid treatment. Reactive Oxygen Species MpV17 mitochondrial inner membrane protein Mus musculus
4 The development of glomerular disease in Mpv17-/- mice was inhibited by scavengers of oxygen radicals (dithiomethylurea) and lipid peroxidation (probucol), but not by steroid treatment. dithiomethylurea MpV17 mitochondrial inner membrane protein Mus musculus
5 Although the glomerular polyanion was greatly reduced in proteinuric Mpv17-/- mice, it was preserved by antioxidative therapy. polyanions MpV17 mitochondrial inner membrane protein Mus musculus
6 These results indicate that the glomerular disease in Mpv17-/- mice qualifies as a model of steroid-resistant focal segmental glomerulosclerosis and that experimental therapies with scavengers of oxygen radicals and lipid peroxidation efficiently ameliorate glomerular damage. Steroids MpV17 mitochondrial inner membrane protein Mus musculus