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Gewählte Publikation:

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Publikationstyp: Zeitschriftenaufsatz
Dokumenttyp: Originalarbeit

Jahr: 2019

AutorInnen: Kaltenecker, D; Themanns, M; Mueller, KM; Spirk, K; Suske, T; Merkel, O; Kenner, L; Luís, A; Kozlov, A; Haybaeck, J; Müller, M; Han, X; Moriggl, R

Titel: Hepatic growth hormone - JAK2 - STAT5 signalling: Metabolic function, non-alcoholic fatty liver disease and hepatocellular carcinoma progression.

Quelle: Cytokine. 2019; 124:154569



Autor/innen der Vetmeduni Vienna:

Kaltenecker Doris
Kenner Lukas
Moriggl Richard
Müller Kristina
Müller Mathias
Spirk Katrin
Suske Tobias
Themanns Madeleine

Beteiligte Vetmed-Organisationseinheiten
Institut für Tierzucht und Genetik, Abteilung für Funktionelle Krebsgenomik
Institut für Pathologie, Abteilung für Labortierpathologie
Institut für Tierzucht und Genetik, Abteilung für Molekulare Genetik


Abstract:
The rising prevalence of obesity came along with an increase in associated metabolic disorders in Western countries. Non-alcoholic fatty liver disease (NAFLD) represents the hepatic manifestation of the metabolic syndrome and is linked to primary stages of liver cancer development. Growth hormone (GH) regulates various vital processes such as energy supply and cellular regeneration. In addition, GH regulates various aspects of liver physiology through activating the Janus kinase (JAK) 2- signal transducer and activator of transcription (STAT) 5 pathway. Consequently, disrupted GH - JAK2 - STAT5 signaling in the liver alters hepatic lipid metabolism and is associated with NAFLD development in humans and mouse models. Interestingly, while STAT5 as well as JAK2 deficiency correlates with hepatic lipid accumulation, recent studies suggest that these proteins have unique ambivalent functions in chronic liver disease progression and tumorigenesis. In this review, we focus on the consequences of altered GH - JAK2 - STAT5 signaling for hepatic lipid metabolism and liver cancer development with an emphasis on lessons learned from genetic knockout models.Copyright © 2018 The Authors. Published by Elsevier Ltd.. All rights reserved.


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