Oxidative stress and glutathione in TGF-beta-mediated fibrogenesis.

Oxidative stress and glutathione in TGF-beta-mediated fibrogenesis.
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DOI:
10.1016/j.freeradbiomed.2009.09.026
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发表时间:
2010-01-01
影响因子:
7.4
通讯作者:
Pravia, K. A. Gaston
Pravia, K. A. Gaston
中科院分区:
医学1区
文献类型:
--
作者:
Liu, R. -M.;Pravia, K. A. Gaston

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Transforming growth factor beta (TGF-β) is the most potent and ubiquitous profibrogenic cytokine and its expression is increased in almost all the fibrotic diseases and in experimental fibrosis models. TGF-β increases ROS production and decreases the concentration of glutathione (GSH), the most abundant intracellular free thiol and an important antioxidant, in various types of cells, which mediates many of TGF-β’s fibrogenic effects. A decreased GSH concentration is also observed in human fibrotic diseases and in experimental fibrosis models. Although the biological significance of GSH depletion in the development of fibrosis remains obscure, GSH and N-acetylcysteine (NAC), a precursor of GSH, have been used in clinics for the treatment of fibrotic diseases. This review summarizes recent findings in the field to address the potential mechanism whereby oxidative stress mediates TGF-β’s fibrogenesis and the potential therapeutic values of antioxidant treatment in fibrotic diseases.
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