The DOI matches its Crossref record; 95 of the 95 references it cites were found in a registry or an index.
Signalling pathways in alcohol-induced liver inflammation
Open accessAbstract
The pathogenesis of alcoholic liver injury involves interactions of several intracellular signalling pathways in different cell types of the liver. Alcohol-induced sensitization of liver macrophages to portal endotoxin/lipopolysaccharide (LPS) is considered a hallmark of alcoholic liver disease (ALD). Intracellular mechanisms associated with LPS-induced signalling play a crucial role in the initiation and progression of alcoholic liver injury, and are being extensively explored. LPS recognition by Toll-like receptor 4 (TLR4) on macrophages and other cell types in the liver, activation of downstream signalling pathways culminating in activation of transcription factors such as NFkappaB, AP-1 leads to increased inflammatory cytokine production in ALD. In addition, LPS-induced MAPK such as ERK and p38 also contribute to liver injury. The importance of alcohol-induced reactive oxygen species and interactions with TLR pathways in macrophages leading to inflammation is becoming increasingly evident. Collectively, these signalling pathways induce pro- and anti-inflammatory cytokines that play an important role in ALD. In this review we describe the key signalling intermediates leading to alcohol-induced inflammation in alcoholic liver disease.
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Arroyo, V., Angeli, P., Moreau, R., Jalan, R., Clària, J., Trebicka, J., Fernández, J., Gustot, T., Caraceni, P., & Bernardi, M. (2021) · Journal of Hepatology · doi:10.1016/j.jhep.2020.11.048 · Cited by 458
Metadata
- Authors
- Mandrekar, P., & Szabo, G.
- Venue
- Journal of Hepatology
- Publisher
- Elsevier BV
- Published
- 2009-06
- Volume
- 50
- Issue
- 6
- Pages
- 1258-1266
- ISSN
- 0168-8278 (ISSN-L)
- OpenAlex
- W2017730825
- Cited by
- 498
- References
- 95
- FWCI
- 18.51
- Type
- journal article
- Language
- en
- Open access
- hybrid
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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.