ArticleScientific reports2019
Oncostatin M exerts a protective effect against excessive scarring by counteracting the inductive effect of TGFβ1 on fibrosis markers.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Cell-based cytokine patch for localized immunomodulation and accelerated healing in rodent and porcine wounds.Nature biomedical engineering · 2026Article
- Combined antagonism of Oncostatin M (OSM) and Interleukin 6 (IL-6) provides both anti-fibrotic and anti-inflammatory benefit in pulmonary fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Advances in Tissue Engineering and Biomaterials for Minimizing Wound Scarring: Current Status and Future Challenges.Journal of functional biomaterials · 2025Review
- Skin tropism during Usutu virus and West Nile virus infection: an amplifying and immunological role.Journal of virology · 2024Article
- Oncostatin M-Enriched Small Extracellular Vesicles Derived from Mesenchymal Stem Cells Prevent Isoproterenol-Induced Fibrosis and Enhance Angiogenesis.International journal of molecular sciences · 2023Article
- The clinical relevance of OSM in inflammatory diseases: a comprehensive review.Frontiers in immunology · 2023Review
- Oncostatin M Counteracts the Fibrotic Effects of TGF-β1 and IL-4 on Nasal-Polyp-Derived Fibroblasts: A Control of Fibrosis in Chronic Rhinosinusitis with Nasal Polyps?International journal of molecular sciences · 2022Article
- Dermal fibroblasts are the key sensors of aseptic skin inflammation through interleukin 1 release by lesioned keratinocytes.Frontiers in immunology · 2022Article
- The Role of Extracellular Matrix in Skin Wound Healing.Journal of clinical medicine · 2021Review
- Cardiac fibrosis.Cardiovascular research · 2021Review
- SHANK2 mutations impair apoptosis, proliferation and neurite outgrowth during early neuronal differentiation in SH-SY5Y cells.Scientific reports · 2021Article
- Role of oncostatin M in the pathogenesis of vernal keratoconjunctivitis: focus on tissue remodeling.Japanese journal of ophthalmology · 2021Article
- Scar-Free Healing: Current Concepts and Future Perspectives.Nanomaterials (Basel, Switzerland) · 2020Review
- Molecular signatures of anthroponotic cutaneous leishmaniasis in the lesions of patients infected with Leishmania tropica.Scientific reports · 2020Article
- RNA Sequencing Keloid Transcriptome Associates Keloids With Th2, Th1, Th17/Th22, and JAK3-Skewing.Frontiers in immunology · 2020Article
- Oncostatin M in the Regulation of Connective Tissue Cells and Macrophages in Pulmonary Disease.Biomedicines · 2019Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wound healing is a complex physiological process that repairs a skin lesion and produces fibrous tissue. In some cases, this process can lead to hypertrophic scars (HS) or keloid scars (KS), for which the pathophysiology remains poorly understood. Previous studies have reported the presence of oncostatin M (OSM) during the wound healing process; however, the role of OSM in pathological scarring remains to be precisely elucidated. This study aims to analyse the presence and involvement of OSM in the pathological scarring process. It was conducted with 18 patients, including 9 patients with hypertrophic scarring and 9 patients with keloid scarring. Histological tissue analysis of HS and KS showed minor differences in the organization of the extracellular matrix, the inflammatory infiltrate and the keratinocyte phenotype. Transcriptomic analysis showed increased expression levels of fibronectin, collagen I, TGFβ1, β-defensin-2 and S100A7 in both pathological samples. OSM expression levels were greater in HS than in KS and control skin. In vitro, OSM inhibited TGFβ1-induced secretion of components of the extracellular matrix by normal and pathological fibroblasts. Overall, we suggest that OSM is involved in pathological wound healing processes by inhibiting the evolution of HS towards KS by controlling the fibrotic effect of TGFβ1.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.