Mechanisms of chronic JAK-STAT3-SOCS3 signaling in obesity

Janus kinase (JAK)-signal transducers and activators of transcription (STAT) signaling pathways are critical for the maintenance of homeostatic and developmental processes; however, deregulation and chronic activation of JAK-STAT3 results in numerous diseases. Among others, obesity is currently bein...

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Autores principales: Wunderlich, Claudia M., Hövelmeyer, Nadine, Wunderlich, F. Thomas
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2013
Materias:
Review
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3710326/
https://www.ncbi.nlm.nih.gov/pubmed/24058813
http://dx.doi.org/10.4161/jkst.23878
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author Wunderlich, Claudia M.
Hövelmeyer, Nadine
Wunderlich, F. Thomas
author_facet Wunderlich, Claudia M.
Hövelmeyer, Nadine
Wunderlich, F. Thomas
author_sort Wunderlich, Claudia M.
collection PubMed
description Janus kinase (JAK)-signal transducers and activators of transcription (STAT) signaling pathways are critical for the maintenance of homeostatic and developmental processes; however, deregulation and chronic activation of JAK-STAT3 results in numerous diseases. Among others, obesity is currently being intensively studied. In obesity, chronic JAK-STAT3 is activated by the CNS by increased circulating leptin levels leading to the development of leptin resistance, whereas in the peripheral organs chronic IL-6-induced JAK-STAT3 impairs insulin action. We report the consequences of chronic JAK-STAT3 induced signaling as present under obese conditions in the main metabolic organs.
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spelling pubmed-37103262013-09-19 Mechanisms of chronic JAK-STAT3-SOCS3 signaling in obesity Wunderlich, Claudia M. Hövelmeyer, Nadine Wunderlich, F. Thomas JAKSTAT Review Janus kinase (JAK)-signal transducers and activators of transcription (STAT) signaling pathways are critical for the maintenance of homeostatic and developmental processes; however, deregulation and chronic activation of JAK-STAT3 results in numerous diseases. Among others, obesity is currently being intensively studied. In obesity, chronic JAK-STAT3 is activated by the CNS by increased circulating leptin levels leading to the development of leptin resistance, whereas in the peripheral organs chronic IL-6-induced JAK-STAT3 impairs insulin action. We report the consequences of chronic JAK-STAT3 induced signaling as present under obese conditions in the main metabolic organs. Landes Bioscience 2013-04-01 2013-04-01 /pmc/articles/PMC3710326/ /pubmed/24058813 http://dx.doi.org/10.4161/jkst.23878 Text en Copyright © 2013 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Review
Wunderlich, Claudia M.
Hövelmeyer, Nadine
Wunderlich, F. Thomas
Mechanisms of chronic JAK-STAT3-SOCS3 signaling in obesity
title Mechanisms of chronic JAK-STAT3-SOCS3 signaling in obesity
title_full Mechanisms of chronic JAK-STAT3-SOCS3 signaling in obesity
title_fullStr Mechanisms of chronic JAK-STAT3-SOCS3 signaling in obesity
title_full_unstemmed Mechanisms of chronic JAK-STAT3-SOCS3 signaling in obesity
title_short Mechanisms of chronic JAK-STAT3-SOCS3 signaling in obesity
title_sort mechanisms of chronic jak-stat3-socs3 signaling in obesity
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3710326/
https://www.ncbi.nlm.nih.gov/pubmed/24058813
http://dx.doi.org/10.4161/jkst.23878
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