Cited by 176Cytokine Signaling Pathways and InteractionsAdipokines, Inflammation, and Metabolic DiseasesRegulation of Appetite and Obesity

Mechanisms of chronic JAK-STAT3-SOCS3 signaling in obesity

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Wunderlich, Claudia M., Hövelmeyer, Nadine, Wunderlich, F. Thomas·2013·JAK-STAT

Abstract

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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Authors
Wunderlich, C. M., Hövelmeyer, N., & Wunderlich, F. T.
Affiliations
Max Planck Society (DE)
Corresponding author
Wunderlich, F. Thomas
Venue
JAK-STAT
Published
2013-04
Volume
2
Issue
2
Pages
e23878
ISSN
  • 2162-3988 (ISSN-L)
  • 2162-3996
OpenAlex
W2082776945
Cited by
176
References
9
Citations by year
2026: 13 · 2025: 13 · 2024: 8 · 2023: 19 · 2022: 17 · 2021: 15 · 2020: 12 · 2019: 9 · 2018: 19 · 2017: 16 · 2016: 11 · 2015: 10 · 2014: 13 · 2013: 1
FWCI
1.23
Type
journal article
Language
en
Open access
Licence
cc-by-nc
Locations
  • JAK-STAT (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Keywords
JAK/STAT3 signaling, obesity, SOCS3, leptin resistance, interleukin-6, insulin resistance, central nervous system

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