ArticleCell research2011
Oncostatin M inhibits myoblast differentiation and regulates muscle regeneration.
Article in Cell research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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
31 citing papers in PubMed, 80 citations in OpenAlex.
- Transcriptomic response of skeletal muscle to acute aerobic versus combined exercise in chronic kidney disease.PloS one · 2026Trial
- miR-203, a tumor suppressor frequently down-regulated by promoter hypermethylation in rhabdomyosarcoma.The Journal of biological chemistry · 2014Trial
- M2 Macrophage-Derived Extracellular Vesicles Reprogram Immature Neutrophils into Anxa1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Autoimmune inflammation as a key risk factor for heart failure with preserved ejection fraction: the different types of inflammation driving to HFpEF.Frontiers in medicine · 2025Review
- Tumor necrosis factor α deficiency promotes myogenesis and muscle regeneration.Zoological research · 2024Article
- Article
- Macrophage scavenger receptor A1 promotes skeletal muscle regeneration after hindlimb ischemia.Journal of biomedical research · 2024Article
- Oncostatin M signaling drives cancer-associated skeletal muscle wasting.Cell reports. Medicine · 2024Article
- Evidence that Alzheimer's Disease Is a Disease of Competitive Synaptic Plasticity Gone Awry.Journal of Alzheimer's disease : JAD · 2024Review
- The therapeutic potential of targeting Oncostatin M and the interleukin-6 family in retinal diseases: A comprehensive review.Open life sciences · 2024Review
- Muscle stem cells as immunomodulator during regeneration.Current topics in developmental biology · 2024Review
- Loss of ZBED6 Protects Against Sepsis-Induced Muscle Atrophy by Upregulating DOCK3-Mediated RAC1/PI3K/AKT Signaling Pathway in Pigs.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Proteoglycan Extracted fromACS omega · 2023Article
- CD34Science advances · 2023Article
- Review
- Exogenous Oncostatin M induces Cardiac Dysfunction, Musculoskeletal Atrophy, and Fibrosis.Cytokine · 2022Article
- The Role of Oxidative Stress in Skeletal Muscle Myogenesis and Muscle Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Article
- Identification of self-regulatory network motifs in reverse engineering gene regulatory networks using microarray gene expression data.IET systems biology · 2019Article
- Induction of muscle stem cell quiescence by the secreted niche factor Oncostatin M.Nature communications · 2018Article
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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncostatin M (OSM) is a cytokine of the interleukin-6 family and plays important roles during inflammation. However, its roles in myoblast differentiation and muscle regeneration remain unexplored. We show here that OSM potently inhibited myoblast differentiation mainly by activating the JAK1/STAT1/STAT3 pathway. OSM downregulated myocyte enhancer-binding factor 2A (MEF2A), upregulated the expression of Id1 and Id2, and inhibited the transcriptional activity of MyoD and MEF2. In addition, OSM also enhanced the expression of STAT3 and OSM receptor, which constituted a positive feedback loop to further amplify OSM-induced signaling. Moreover, we found that STAT1 physically associated with MEF2 and repressed its transcriptional activity, which could account for the OSM-mediated repression of MEF2. Although undetectable in normal muscles in vivo, OSM was rapidly induced on muscle injury and then promptly downregulated just before the majority of myoblasts differentiate. Prolonged expression of OSM in muscles compromised the regeneration process without affecting myoblast proliferation, suggesting that OSM functions to prevent proliferating myoblasts from premature differentiation during the early phase of muscle regeneration.
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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.