Does nO mediate antifibrotic actions of L-arginine supplementation following induction of anti-thy1 glomerulonephritis?
The present study shows that L-arginine's antifibrotic action in normotensive anti-thy1 GN is mainly mediated by endogenous production of NO. The data suggest that NO limits in vivo TGF-beta overexpression in a pressure-independent manner and that NO donors may be of benefit in the treatment of human fibrotic renal disease.
The quality of HSCs from low mobilizers was comparable to HSCs from high mobilizers.