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• W2096808011 abstract "Innate immune signaling associated with Toll-like receptors (TLRs) is a key pathway involved in the progression of liver fibrosis. In this study, we reported that TLR2 is required for hepatic fibrogenesis induced by carbon tetrachloride (CCl4). After CCl4 treatment, TLR2−/− mice had reduced liver enzyme levels, diminished collagen deposition, decreased inflammatory infiltration and impaired activation of hepatic stellate cells (HSCs) than wild type (WT) mice. Furthermore, after CCl4 treatment, TLR2−/− mice demonstrated downregulated expression of profibrotic and proinflammatory genes and impaired mitogen-activated protein kinases (MAPK) and nuclear factor kappa B (NF-κB) activation than WT mice. Collectively, our data indicate that TLR2 deficiency protects against CCl4-induced liver fibrosis." @default.
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• W2096808011 date "2014-05-08" @default.
• W2096808011 modified "2023-10-17" @default.
• W2096808011 title "Toll like receptor 2 knock-out attenuates carbon tetrachloride (CCl₄ )-induced liver fibrosis by downregulating MAPK and NF-κB signaling pathways" @default.
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• W2096808011 doi "https://doi.org/10.1016/j.febslet.2014.04.042" @default.
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