ArticleBioMed research international2015
OSM Enhances Angiogenesis and Improves Cardiac Function after Myocardial Infarction.
Article in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Proteins targeting ischaemic-reperfusion injury and repair after myocardial infarction: a systematic literature review.Cardiovascular research · 2026Pooled it
- The Role of the OSM/OSMRβ Axis in Chronic Liver Disease Progression and Hepatocellular Carcinoma Development: A Focus on MASLD/MASH.International journal of molecular sciences · 2026Review
- Article
- A bibliometric analysis of trends and hotspots in Oncostatin M.Discover oncology · 2026Article
- 3D-printed PRP-infused double-network hydrogels orchestrate inflammation resolution and vascular regeneration in infected wounds.Materials today. Bio · 2026Article
- Clinical significance of miR-548a-3p and its potential role in acute respiratory distress syndrome complicated with pulmonary fibrosis via OSM.BMC immunology · 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
- Causal effects of inflammatory cytokines on hemangioma mediated by blood metabolites: A two-step Mendelian randomization study.Journal of medical biochemistry · 2025Article
- Serum proteomics links the cardiorespiratory biomarkers CTRC, OSM, and MMP-10 to exacerbation severity and number in patients with COPD.Clinical science (London, England : 1979) · 2025Article
- Review
- Oncostatin M Reduces Pathological Neovascularization in the Retina Through Müller Cell Activation.Investigative ophthalmology & visual science · 2024Article
- Oncostatin M mediates cardioprotection via angiogenesis in ischemic heart disease.American heart journal plus : cardiology research and practice · 2023Article
- Oncostatin M-Enriched Small Extracellular Vesicles Derived from Mesenchymal Stem Cells Prevent Isoproterenol-Induced Fibrosis and Enhance Angiogenesis.International journal of molecular sciences · 2023Article
- Extracellular vesicle-derived circCEBPZOS attenuates postmyocardial infarction remodeling by promoting angiogenesis via the miR-1178-3p/PDPK1 axis.Communications biology · 2023Article
- Identification of biomarkers related to copper metabolism in patients with pulmonary arterial hypertension.BMC pulmonary medicine · 2023Article
- The clinical relevance of OSM in inflammatory diseases: a comprehensive review.Frontiers in immunology · 2023Review
- Exogenous Oncostatin M induces Cardiac Dysfunction, Musculoskeletal Atrophy, and Fibrosis.Cytokine · 2022Article
- Association of increased oncostatin M with adverse left ventricular remodeling in patients with myocardial infarction.Journal of medical biochemistry · 2022Article
- The Role of Oncostatin M and Its Receptor Complexes in Cardiomyocyte Protection, Regeneration, and Failure.International journal of molecular sciences · 2022Review
- Concomitant Activation of OSM and LIF Receptor by a Dual-Specific hlOSM Variant Confers Cardioprotection after Myocardial Infarction in Mice.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncostatin M (OSM) has been reported to stimulate angiogenesis by upregulating VEGF and bFGF, implying that it could be a therapeutic strategy in treating ischemic diseases. The present study was aimed at investigating whether OSM could improve cardiac function via prompting angiogenesis following myocardial infarction (MI). Wild type (WT) and Oβ knock-out (Oβ (-/-)) mice were, respectively, randomized into sham group, MI + vehicle group, and MI + OSM group. WT mice displayed significantly impaired cardiac function after MI. OSM treatment attenuated cardiac dysfunction in WT MI mice, while Oβ deletion abrogated the protective effects. Besides, OSM attenuated heart hypertrophy and pulmonary congestion evidenced by decreased heart weight/body weight and lung weight/body weight ratio. Further, reduction of apoptosis and fibrosis in infarct border zone was observed in OSM treated WT MI mice compared with vehicle. Moreover, in WT mice subjected to MI, OSM treatment significantly increased capillary density along with upregulation of p-Akt and angiogenic factors VEGF and bFGF in comparison with vehicle, and this phenomenon was not found in Oβ (-/-) mice. In conclusion, OSM treatment preserved cardiac function, inhibited apoptosis and fibrosis, and stimulated angiogenesis via upregulating VEGF and bFGF in infarct border zone of ischemic myocardium, indicating that OSM could be a novel therapeutic target for MI.
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