ArticleBMC gastroenterology2009
Liver fibrosis secondary to bile duct injury: correlation of Smad7 with TGF-beta and extracellular matrix proteins.
Article in BMC gastroenterology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- TGF-β signaling is activated in patients with chronic HBV infection and repressed by SMAD7 overexpression after successful antiviral treatment.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016Article
- Autophagy inhibition of hsa-miR-19a-3p/19b-3p by targeting TGF-β R II during TGF-β1-induced fibrogenesis in human cardiac fibroblasts.Scientific reports · 2016Article
- Manual therapy as an effective treatment for fibrosis in a rat model of upper extremity overuse injury.Journal of the neurological sciences · 2016Article
- Astragalus and Paeoniae radix rubra extract inhibits liver fibrosis by modulating the transforming growth factor‑β/Smad pathway in rats.Molecular medicine reports · 2015Article
- TGF-β and TGF-β/Smad signaling in the interactions between Echinococcus multilocularis and its hosts.PloS one · 2013Article
- YKL-40 expression in CD14⁺ liver cells in acute and chronic injury.World journal of gastroenterology · 2011Article
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Authors and funding
11 authors.
Funding
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Abstract
backgroundLiver fibrosis is the result of continuous liver injury stemming from different etiological factors. Bile duct injury induces an altered expression of TGF-beta, which has an important role in liver fibrosis because this cytokine induces the expression of target genes such as collagens, PAI-1, TIMPs, and others that lead to extracellular matrix deposition. Smad7 is the principal inhibitor that regulates the target gene transcription of the TGF-beta signaling. The aim of the study was to determine whether Smad7 mRNA expression correlates with the gene expression of TGF-beta, Col I, Col III, Col IV, or PAI-1 in liver fibrosis secondary to bile duct injury (BDI).
resultsSerum TGF-beta concentration was higher in BDI patients (39 296 pg/ml) than in liver donors (9008 pg/ml). Morphometric analysis of liver sections showed 41.85% of tissue contained fibrotic deposits in BDI patients. mRNA expression of Smad7, Col I, and PAI-1 was also significantly higher (P < 0.05) in patients with BDI than in controls. Smad7 mRNA expression correlated significantly with TGF-beta concentration, Col I and Col III expression, and the amount of fibrosis.
conclusionWe found augmented serum concentration of TGF-beta and an increase in the percentage of fibrotic tissue in the liver of BDI patients. Contrary to expected results, the 6-fold increase in Smad7 expression did not inhibit the expression of TGF-beta, collagens, and PAI-1. We also observed greater expression of Col I and Col III mRNA in BDI patients and significant correlations between their expression and TGF-beta concentration and Smad7 mRNA expression.
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