title: P(URI)fying Novel Drivers of NASH and HCC: A Feedforward Loop of IL17A via White Adipose Tissue.
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.
authors.affiliation: Institute of Surgical Pathology, University and University Hospital Zurich, Zurich 8091, Switzerland.
authors.forename: Achim
authors.initials: A
authors.lastname: Weber
authors.affiliation: 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: m.heikenwaelder@dkfz.de.
authors.forename: Mathias
authors.initials: M
authors.lastname: Heikenwalder
mesh_terms: D052436:Adipose Tissue, White / Q000378:metabolism; D006528:Carcinoma, Hepatocellular / Q000378:metabolism*; D005234:Fatty Liver; D006801:Humans; D008113:Liver Neoplasms / Q000378:metabolism*; D065626:Non-alcoholic Fatty Liver Disease / Q000378:metabolism