| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 9308462 | Kidney International | 2005 | 15 Pages |
Abstract
Glomerular and tubulointerstitial soluble guanylate cyclase activity are discordantly altered in anti-thy1-induced chronic glomerulosclerosis. Stimulation of soluble guanylate cyclase signaling by Bay 41-2272 limits the progressive course of this model toward tubulointerstitial fibrosis and impaired renal function at least in part in a blood pressure-independent manner. The results suggest that soluble guanylate cyclase activation counteracts fibrosis and progression in chronic renal disease.
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Authors
Yingrui Wang, Stephanie Kramer, Tanja Loof, Sebastian Martini, Susanne Kron, Hiroshi Kawachi, Fuijo Shimizu, Hans-H Neumayer, Harm Peters,