2026-04-26T23:10:57Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/174032024-11-29T19:48:29Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597
Repisalud
author
Gomes, Ana L
author
Teijeiro, Ana
author
Burén, Stefan
author
Tummala, Krishna S
author
Yilmaz, Mahmut
author
Waisman, Ari
author
Theurillat, Jean-Philippe
author
Perna, Cristian
author
Djouder, Nabil
funder
Ministerio de Economía y Competitividad (España)
funder
European Foundation for the Study of Diabetes
funder
Worldwide Cancer Research
2024-02-01T09:48:49Z
2024-02-01T09:48:49Z
2016-07-11
Cancer Cell . 2016;30(1):161-175.
http://hdl.handle.net/20.500.12105/17403
27411590
10.1016/j.ccell.2016.05.020
1878-3686
Cancer cell
Obesity increases hepatocellular carcinoma (HCC) risks via unknown mediators. We report that hepatic unconventional prefoldin RPB5 interactor (URI) couples nutrient surpluses to inflammation and non-alcoholic steatohepatitis (NASH), a common cause of HCC. URI-induced DNA damage in hepatocytes triggers inflammation via T helper 17 (Th17) lymphocytes and interleukin 17A (IL-17A). This induces white adipose tissue neutrophil infiltration mediating insulin resistance (IR) and fatty acid release, stored in liver as triglycerides, causing NASH. NASH and subsequently HCC are prevented by pharmacological suppression of Th17 cell differentiation, IL-17A blocking antibodies, and genetic ablation of the IL-17A receptor in myeloid cells. Human hepatitis, fatty liver, and viral hepatitis-associated HCC exhibit increased IL-17A correlating positively with steatosis. IL-17A blockers may prevent IR, NASH, and HCC in high-risk patients.
eng
Metabolic Inflammation-Associated IL-17A Causes Non-alcoholic Steatohepatitis and Hepatocellular Carcinoma.
journal article
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metabolicinflammationassociated-2016.pdf
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https://repisalud.isciii.es/bitstreams/229f28cf-ac2a-4b9f-aeaa-4a96cfcdd640/download
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metabolicinflammationassociated-2016.pdf.txt