Oxidative stress and glutathione in TGF-β-mediated fibrogenesis

被引:377
作者
Liu, R. -M. [1 ]
Pravia, K. A. Gaston
机构
[1] Univ Alabama Birmingham, Dept Environm Hlth Sci, Sch Publ Hlth, Birmingham, AL 35294 USA
关键词
TGF-beta; Oxidative stress; Fibrosis; Glutathione; Free radicals; GROWTH-FACTOR-BETA; IDIOPATHIC PULMONARY-FIBROSIS; EPITHELIAL-MESENCHYMAL TRANSITION; ORAL N-ACETYLCYSTEINE; INDUCED LUNG FIBROSIS; PLASMINOGEN-ACTIVATOR INHIBITOR-1; RESPIRATORY-DISTRESS-SYNDROME; OXYGEN SPECIES PRODUCTION; PROTEIN PHOSPHATASE 2A; ALCOHOLIC-LIVER-DISEASE;
D O I
10.1016/j.freeradbiomed.2009.09.026
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Transforming growth factor beta (TGF-beta) 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-beta increases reactive oxygen species production and decreases the concentration of glutathione (GSH). the most abundant intracellular free thiol and an important antioxidant. which mediates many of the fibrogenic effects of TGF-beta in various types of cells. 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, 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 fibrogenesis induced by TGF-beta and the potential therapeutic value of antioxidant treatment in fibrotic diseases. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:1 / 15
页数:15
相关论文
共 339 条
[1]
Peripheral blood fibrocytes: Differentiation pathway and migration to wound sites [J].
Abe, R ;
Donnelly, SC ;
Peng, T ;
Bucala, R ;
Metz, CN .
JOURNAL OF IMMUNOLOGY, 2001, 166 (12) :7556-7562
[2]
Chrysotile-mediated imbalance in the glutathione redox system in the development of pulmonary injury [J].
Abidi, P ;
Afaq, F ;
Arif, JM ;
Lohani, M ;
Rahman, Q .
TOXICOLOGY LETTERS, 1999, 106 (01) :31-39
[3]
Oxidant stress is a significant feature of primary biliary cirrhosis [J].
Aboutwerat, A ;
Pemberton, PW ;
Smith, A ;
Burrows, PC ;
McMahon, RFT ;
Jain, SK ;
Warnes, TW .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, 2003, 1637 (02) :142-150
[5]
Mitochondrial and microsomal derived reactive oxygen species mediate apoptosis induced by transforming growth factor-β1 in immortalized rat hepatocytes [J].
Albright, CD ;
Salganik, RI ;
Craciunescu, CN ;
Mar, MH ;
Zeisel, SH .
JOURNAL OF CELLULAR BIOCHEMISTRY, 2003, 89 (02) :254-261
[6]
Ali Mohamed A, 2004, Egypt J Immunol, V11, P83
[7]
Endogenous TGF-β activation by reactive oxygen species is key to Foxp3 induction in TCR-stimulated and HIV-I-infected human CD4+CD25- T cells [J].
Amarnath, Shoba ;
Dong, Li ;
Li, Jun ;
Wu, Yuntao ;
Chen, WanJun .
RETROVIROLOGY, 2007, 4 (1)
[8]
Transforming growth factor-β signaling mediates hypoxia-induced pulmonary arterial remodeling and inhibition of alveolar development in newborn mouse lung [J].
Ambalavanan, Namasivayam ;
Nicola, Teodora ;
Hagood, James ;
Bulger, Arlene ;
Serra, Rosa ;
Murphy-Ullrich, Joanne ;
Oparil, Suzanne ;
Chen, Yiu-Fai .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2008, 295 (01) :L86-L95
[9]
Anti-fibrotic effect of meloxicam in a murine lung fibrosis model [J].
Arafa, Hossam M. M. ;
Abdel-Wahab, Mohamed H. ;
El-Shafeey, Mohamed F. ;
Badary, Osama A. ;
Hamada, Farid M. A. .
EUROPEAN JOURNAL OF PHARMACOLOGY, 2007, 564 (1-3) :181-189
[10]
Oxidative stress triggers cardiac fibrosis in the heart of diabetic rats [J].
Aragno, Manuela ;
Mastrocola, Raffaella ;
Alloatti, Giuseppe ;
Vercellinatto, Ilenia ;
Bardini, Paola ;
Geuna, Stefano ;
Catalano, Maria Graziella ;
Danni, Oliviero ;
Boccuzzi, Giuseppe .
ENDOCRINOLOGY, 2008, 149 (01) :380-388