The DOI matches its Crossref record; 94 of the 94 references it cites were found in a registry or an index.
Interleukin‐1 and inflammasomes in alcoholic liver disease/acute alcoholic hepatitis and nonalcoholic fatty liver disease/nonalcoholic steatohepatitis
Abstract
Both alcoholic liver disease (ALD) and nonalcoholic fatty liver disease are characterized by massive lipid accumulation in the liver accompanied by inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma in a substantial subgroup of patients. At several stages in these diseases, mediators of the immune system, such as cytokines or inflammasomes, are crucially involved. In ALD, chronic ethanol exposure sensitizes Kupffer cells to activation by lipopolysaccharides through Toll‐like receptors, e.g., Toll‐like receptor 4. This sensitization enhances the production of various proinflammatory cytokines such as interleukin‐1 (IL‐1) and tumor necrosis factor‐alpha, thereby contributing to hepatocyte dysfunction, necrosis, and apoptosis and the generation of extracellular matrix proteins leading to fibrosis/cirrhosis. Indeed, neutralization of IL‐1 by IL‐1 receptor antagonist has recently been shown to potently prevent liver injury in murine models of ALD. As IL‐1 is clearly linked to key clinical symptoms of acute alcoholic hepatitis such as fever, neutrophilia, and wasting, interfering with the IL‐1 pathway might be an attractive treatment strategy in the future. An important role for IL‐1‐type cytokines and certain inflammasomes has also been demonstrated in murine models of nonalcoholic fatty liver disease. IL‐1‐type cytokines can regulate hepatic steatosis; the NLR family pyrin domain containing 3 inflammasome is critically involved in metabolic dysregulation. Conclusion: IL‐1 cytokine family members and various inflammasomes mediate different aspects of both ALD and nonalcoholic fatty liver disease. (H epatology 2016;64:955‐965)
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Martinon, F., Burns, K., & Tschopp, J. (2002) · Molecular Cell · doi:10.1016/s1097-2765(02)00599-3 · Cited by 6,066
Immunological and inflammatory functions of the interleukin-1 family
Dinarello, C. A. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132612 · Cited by 3,466
The NLRP3 inflammasome instigates obesity-induced inflammation and insulin resistance
Vandanmagsar, B., Youm, Y.-H., Ravussin, A., Galgani, J. E., Stadler, K., Mynatt, R. L., Ravussin, E., Stephens, J. M., & Dixit, V. D. (2011) · Nature Medicine · doi:10.1038/nm.2279 · Cited by 2,655
Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis
Tilg, H., & Moschen, A. R. (2010) · Hepatology · doi:10.1002/hep.24001 · Cited by 2,548
Self-citationInflammasome-mediated dysbiosis regulates progression of NAFLD and obesity
Henao-Mejia, J., Elinav, E., Jin, C., Hao, L., Mehal, W. Z., Strowig, T., Thaiss, C. A., Kau, A. L., Eisenbarth, S. C., Jurczak, M. J., et al. (2012) · Nature · doi:10.1038/nature10809 · Cited by 2,435
What we talk about when we talk about fat
Rosen, E. D., & Spiegelman, B. M. (2014) · Cell · doi:10.1016/j.cell.2013.12.012 · Cited by 2,373
The interleukin-1 family: back to the future
Garlanda, C., Dinarello, C. A., & Mantovani, A. (2013) · Immunity · doi:10.1016/j.immuni.2013.11.010 · Cited by 1,945 · cited 3×
“These mediators are mainly proinflammatory but can also be anti-inflammatory and are important in almost all inflammatory conditions, exerting their specific effects through IL-1Rs 1-10.((6)) They are also involved in the differentiation and function of many innate and lymphoid cells, direct many complex inflammatory…”
BackgroundInfluentialTreating inflammation by blocking interleukin-1 in a broad spectrum of diseases
Dinarello, C. A., Simon, A., & van der Meer, J. W. M. (2012) · Nature Reviews Drug Discovery · doi:10.1038/nrd3800 · Cited by 1,768
Progression of NAFLD to diabetes mellitus, cardiovascular disease or cirrhosis
Anstee, Q. M., Targher, G., & Day, C. P. (2013) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/nrgastro.2013.41 · Cited by 1,747
Hoffman, H. M., Mueller, J. L., Broide, D. H., Wanderer, A. A., & Kolodner, R. D. (2001) · Nature Genetics · doi:10.1038/ng756 · Cited by 1,682
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Immunotherapies for hepatocellular carcinoma
Llovet, J. M., Castet, F., Heikenwalder, M., Maini, M. K., Mazzaferro, V., Pinato, D. J., Pikarsky, E., Zhu, A. X., & Finn, R. S. (2022) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-021-00573-2 · Cited by 1,843
The gut-liver axis and the intersection with the microbiome
Tripathi, A., Debelius, J., Brenner, D. A., Karin, M., Loomba, R., Schnabl, B., & Knight, R. (2018) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-018-0011-z · Cited by 1,480
Liver Macrophages in Tissue Homeostasis and Disease
Krenkel, O., & Tacke, F. (2017) · Nature Reviews Immunology · doi:10.1038/nri.2017.11 · Cited by 1,424
Recovery of ethanol-induced Akkermansia muciniphila depletion ameliorates alcoholic liver disease
Grander, C., Adolph, T. E., Wieser, V., Lowe, P., Wrzosek, L., Gyongyosi, B., Ward, D. V., Grabherr, F., Gerner, R. R., Pfister, A., et al. (2018) · Gut · doi:10.1136/gutjnl-2016-313432 · Cited by 618
Self-citation
Metadata
- Authors
- Tilg, H., Moschen, A. R., & Szabo, G.
- Venue
- Hepatology
- Published
- 2016-03-09
- Volume
- 64
- Issue
- 3
- Pages
- 955-965
- ISSN
- 0270-9139 (ISSN-L)
- 1527-3350
- OpenAlex
- W2514873437
- Cited by
- 319
- References
- 94
- FWCI
- 26.32
- Type
- journal article
- Language
- en
- Open access
- closed
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