| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3296106 | Gastroenterology | 2010 | 11 Pages |
Abstract
These findings provide further evidence to support the hypothesis that HCV enhances hepatic fibrosis progression through the generation of ROS and induction of TGF-β1. Strategies to limit the viral induction of oxidative stress appear to be warranted to inhibit fibrogenesis.
Keywords
FBSGAPDHERKECLSP600125JnkTGF-β1SB 203580LY 294002HSCPI3KDPIc-Jun N-terminal kinaseDMSONFκBp38 MAPKshort interfering RNAROSsiRNAElectrochemiluminescenceTransforming growth factor β1diphenyliodoniumDimethyl sulfoxidefetal bovine serumHepatic stellate cellnuclear factor κBPhosphoinositol-3 kinasenegativenegHCVHepatitis C viruspolymerase chain reactionPCRp38 mitogen-activated protein kinaseextracellular signal-regulated kinaseglyceraldehyde-3-phosphate dehydrogenaseReactive oxygen species
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Authors
Wenyu Lin, Wei-Lun Tsai, Run-Xuan Shao, Guoyang Wu, Lee F. Peng, Lydia L. Barlow, Woo Jin Chung, Leiliang Zhang, Hong Zhao, Jae-Young Jang, Raymond T. Chung,