The DOI matches its Crossref record; 193 of the 193 references it cites were found in a registry or an index.
Toll-like receptors as targets in chronic liver diseases
Open accessAbstract
Toll-like receptors (TLRs) recognise pathogen-associated molecular patterns (PAMPs) to detect the presence of pathogens. In addition to their role in innate immunity, TLRs also play a major role in the regulation of inflammation, even under sterile conditions such as injury and wound healing. This involvement has been suggested to depend, at least in part, on the ability of TLRs to recognise several endogenous TLR ligands termed damage-associated molecular patterns (DAMPs). The liver not only represents a major target of bacterial PAMPs in many disease states but also upregulates several DAMPs following injury. Accordingly, TLR-mediated signals have been implicated in a number of chronic liver diseases. Here, we will summarise recent findings on the role TLRs and TLR ligands in the pathophysiology of liver fibrosis and cirrhosis, viral hepatitis, alcoholic liver disease, non-alcoholic fatty liver disease and hepatocellular carcinoma, and highlight the potential role of TLR agonists, antagonists and probiotics for the treatment of chronic liver disease.
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Cites
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Cited by
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Self-citationImmunology in the liver — from homeostasis to disease
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Liver fibrosis: Pathophysiology, pathogenetic targets and clinical issues
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Metadata
- Authors
- Mencin, A., Kluwe, J., & Schwabe, R. F.
- Venue
- Gut
- Publisher
- BMJ
- Published
- 2009-04-09
- Volume
- 58
- Issue
- 5
- Pages
- 704-720
- ISSN
- 0017-5749 (ISSN-L)
- 1468-3288
- OpenAlex
- W2151608099
- Cited by
- 329
- References
- 193
- FWCI
- 10.69
- Type
- journal article
- Language
- en
- Open access
- green
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
