| First Author | Ji L | Year | 2014 |
| Journal | FEBS Lett | Volume | 588 |
| Issue | 12 | Pages | 2095-100 |
| PubMed ID | 24815695 | Mgi Jnum | J:211658 |
| Mgi Id | MGI:5575820 | Doi | 10.1016/j.febslet.2014.04.042 |
| Citation | Ji L, et al. (2014) Toll like receptor 2 knock-out attenuates carbon tetrachloride (CCl4)-induced liver fibrosis by downregulating MAPK and NF-kappaB signaling pathways. FEBS Lett 588(12):2095-100 |
| abstractText | 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-kappaB) activation than WT mice. Collectively, our data indicate that TLR2 deficiency protects against CCl4-induced liver fibrosis. |
