Cited by 86Cytokine Signaling Pathways and InteractionsLiver physiology and pathologyTGF-β signaling in diseases

Oncostatin M and its role in fibrosis

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Stawski, Lukasz, Trojanowska, Maria·2019·Connective Tissue Research

Abstract

Oncostain M, a member of the IL-6 family of cytokines, is produced by immune cells in response to infections and tissue injury. OSM has a broad, often context-dependent effect on various cellular processes including differentiation, hematopoiesis, cell proliferation, and cell survival. OSM signaling is initiated by binding to type I (LIFRβ/gp130) or type II (OSMRβ/gp130) receptor complexes and involves activation of Janus kinase/signal transducer and activator of transcription, mitogen-activated protein kinase, and phosphatidylinositol-3-kinase. High levels of OSM have been detected in many chronic inflammatory conditions characterized by fibrosis, giving a rationale to target OSM for the treatment of these diseases. Here we discuss the current knowledge on the role of OSM in various stages of the fibrotic process including inflammation, vascular dysfunction, and activation of fibroblasts.

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Crossref · 10.1080/03008207.2018.1500558

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  • Phosphorylated STAT-3 is increased in IPF patient biopsies and in mice with bleomycin-induced pulmonary fibrosis.

    “STAT is a downstream signaling molecule from JAK activation with seven subtypes: phosphorylated STAT-3 is elevated in biopsies of patients with IPF and in mice with bleomycin induced pulmonary fibrosis. [174–177]”

    From Emerging pharmacological options in the treatment of idiopathic pulmonary fibrosis (IPF) (2024) · cites this paper as [174]

    The Oncostatin M signaling section (page unavailable) describes STAT3 activation downstream of JAK, but does not report phosphorylated STAT3 levels in IPF biopsies. The Activation of the inflammatory cells section reports increased OSM and LIF mRNA in bleomycin-induced lung fibrosis, not increased phosphorylated STAT3. Searches for IPF biopsies and STAT3 phosphorylation found no passage establishing either claimed observation. (LLM, conf=0.74)

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Authors
Stawski, L., & Trojanowska, M.
Affiliations
Boston University (US)
Corresponding author
Trojanowska, Maria
Venue
Connective Tissue Research
Published
2018-07-30
Volume
60
Issue
1
Pages
40-49
ISSN
  • 0300-8207 (ISSN-L)
  • 1607-8438
OpenAlex
W2887224378
Cited by
86
References
117
Citations by year
2026: 10 · 2025: 9 · 2024: 12 · 2023: 22 · 2022: 11 · 2021: 12 · 2020: 7 · 2019: 2 · 2018: 1
FWCI
0.57
Type
journal article
Language
en
Open access
Locations
  • Connective Tissue Research (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (RO1 AR42334-19)
  • NIH (T32 5T32AR007598-19)
Topics
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
Keywords
oncostatin M, IL-6 family cytokines, fibrosis, chronic inflammation, vascular dysfunction, fibroblast activation, gp130, JAK/STAT signaling, MAPK signaling, PI3K signaling, cytokine signaling
MeSH terms
Animals, Fibrosis, Humans, Inflammation, Models, Biological, Signal Transduction, Oncostatin M, Vascular System Injuries

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