ArticleAmerican journal of translational research2021
Oncostatin M promotes infarct repair and improves cardiac function after myocardial infarction.
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- A bibliometric analysis of trends and hotspots in Oncostatin M.Discover oncology · 2026Article
- Gaps in maternal-fetal interface rejection response: chronic histiocytic intervillositis.Frontiers in immunology · 2025Review
- Oncostatin M-Enriched Small Extracellular Vesicles Derived from Mesenchymal Stem Cells Prevent Isoproterenol-Induced Fibrosis and Enhance Angiogenesis.International journal of molecular sciences · 2023Article
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial infarction (MI) is one of the leading causes of morbidity and mortality worldwide. The immune response plays a central role in post-MI cardiac repair. A growing body of evidence suggests that oncostatin M (OSM), a pleiomorphic cytokine of the interleukin (IL)-6 family, participates in the cardiac healing and remodeling process. However, previous studies have shown inconsistent results, and the exact mechanisms underlying this process have not yet been fully elucidated. We verified whether OSM is involved in the healing process and cardiac remodeling after MI and sought to explore its potential mechanisms. Our data implied OSM's role in facilitating the post-MI healing process in mice, manifested by improved cardiac functional performance and a reduction in fibrotic changes. Furthermore, our flow cytometry analysis revealed that OSM influences the dynamics of cardiac monocytes and macrophages. In mice with a blunted C-X-C motif receptor (CCR)2 signaling pathway, OSM reserved its protective roles and polarized cardiac macrophages toward a reparative phenotype. Moreover, OSM reduced the number of matrix metalloproteinase (MMP)-9
Indexed as
Identifiers
34786061PMC8581943W3211458112What OpenQuestion holds
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.