Oncostatin M and its role in fibrosis
Open accessAbstract
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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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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Cyclooxygenase‐2 activity is necessary for the angiogenic properties of oncostatin M
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Smyth, D. C., Kerr, C. L., & Richards, C. D. (2006) · The Journal of Immunology · doi:10.4049/jimmunol.177.12.8740 · Cited by 30 · see citing works
Negative regulation of onconstatin M signaling by suppressor of cytokine signaling (SOCS-3).
Magrangeas, F., Boisteau, O., DENIS, S., et al. (2001) · PubMed · Cited by 29 · see citing works
Oncostatin M inhibits TGF-β1-induced CTGF expression via STAT3 in human proximal tubular cells
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Potential of Oncostatin M to accelerate diabetic wound healing
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Oncostatin M regulates endothelin-1 production in human endothelial cells
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Emerging pharmacological options in the treatment of idiopathic pulmonary fibrosis (IPF)
Aribindi, K., Liu, G. Y., & Albertson, T. E. (2024) · Expert Review of Clinical Pharmacology · doi:10.1080/17512433.2024.2396121 · Cited by 17 · see citing works
- Authors
- Stawski, L., & Trojanowska, M.
- Affiliations
- Boston University (US)
- Corresponding author
- Trojanowska, Maria
- ORCID
- Trojanowska, Maria
- Venue
- Connective Tissue Research
- Publisher
- Informa UK Limited
- Published
- 2018-07-30
- Volume
- 60
- Issue
- 1
- Pages
- 40-49
- ISSN
- 0300-8207 (ISSN-L)
- 1607-8438
- PMC
- PMC6349219
- 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
- green
- www.ncbi.nlm.nih.gov
- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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