P(URI)fying Novel Drivers of NASH and HCC: A Feedforward Loop of IL17A via White Adipose Tissue

Achim Weber; Mathias Heikenwalder

doi:10.1016/j.ccell.2016.06.010

P(URI)fying Novel Drivers of NASH and HCC: A Feedforward Loop of IL17A via White Adipose Tissue

Cancer Cell. 2016 Jul 11;30(1):15-17. doi: 10.1016/j.ccell.2016.06.010.

Authors

Achim Weber¹, Mathias Heikenwalder²

Affiliations

¹ Institute of Surgical Pathology, University and University Hospital Zurich, Zurich 8091, Switzerland.
² Institute of Virology, Technische Universität München/Helmholtz Zentrum München, Munich 81675, Germany; Division of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ), Heidelberg 69120, Germany. Electronic address: [email protected].

PMID: 27411585
DOI: 10.1016/j.ccell.2016.06.010

Abstract

How obesity and metabolic syndrome trigger non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC) remains elusive. In this issue, Gomes and colleagues describe that nutrient surplus induces hepatic URI expression, triggering genotoxicity and IL17A expression, thus leading to insulin resistance, NASH, and HCC. IL17A signaling blockers might become a readily translatable therapy.

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MeSH terms

Adipose Tissue, White / metabolism
Carcinoma, Hepatocellular / metabolism*
Fatty Liver
Humans
Liver Neoplasms / metabolism*
Non-alcoholic Fatty Liver Disease / metabolism