ArticleMolecular endocrinology (Baltimore, Md.)2011
TGF-β inhibits muscle differentiation by blocking autocrine signaling pathways initiated by IGF-II.
Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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
27 citing papers in PubMed, 41 citations in OpenAlex.
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- Regenerative Medicine: Advanced Therapy for Muscle Tissue Restoration.International journal of molecular sciences · 2026Review
- Effects of Nintedanib on Orofacial Fibroblasts and Myoblasts.Biomolecules · 2026Article
- Smad2/3 Signaling Mediates the Atrophic Response in Vocal Fold Myoblasts In Vitro.The Laryngoscope · 2026Article
- Transcriptomics-based analysis of muscle injury mechanism mediated by inflammatory imbalance in the Duchenne muscular dystrophy muscle microenvironment.Frontiers in neurology · 2026Article
- Dairy byproducts as sustainable alternatives to FCS in 2D and 3D skeletal muscle cell cultures.Bioresources and bioprocessing · 2025Article
- Review
- Effect of transforming growth factor beta receptor I inhibitors on myotube formation in vitro.Scientific reports · 2025Article
- The role of inner nuclear membrane protein emerin in myogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- The effects of TGF-β receptor I inhibitors on myofibroblast differentiation and myotube formation.Frontiers in cell and developmental biology · 2025Article
- Construction of Engineered Muscle Tissue Consisting of Myotube Bundles in a Collagen Gel Matrix.Gels (Basel, Switzerland) · 2023Article
- Genetic Modifiers and Phenotype of Duchenne Muscular Dystrophy: A Systematic Review and Meta-Analysis.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Review
- Micro-Ribonucleic Acid-216a Regulates Bovine Primary Muscle Cells Proliferation and DifferentiationFrontiers in genetics · 2019Article
- Article
- Follistatin N terminus differentially regulates muscle size and fat in vivo.Experimental & molecular medicine · 2017Article
- MAPK signaling pathways and HDAC3 activity are disrupted during differentiation of emerin-null myogenic progenitor cells.Disease models & mechanisms · 2017Article
- Separating myoblast differentiation from muscle cell fusion using IGF-I and the p38 MAP kinase inhibitor SB202190.American journal of physiology. Cell physiology · 2015Article
- Article
- Extracellular deposition of matrilin-2 controls the timing of the myogenic program during muscle regeneration.Journal of cell science · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Skeletal muscle differentiation and regeneration are regulated by interactions between exogenous hormone- and growth factor-activated signaling cascades and endogenous muscle-specific transcriptional programs. IGF-I and IGF-II can promote muscle differentiation in vitro and can enhance muscle maintenance and repair in vivo. In contrast, members of the TGF-β superfamily prominently inhibit muscle differentiation and regeneration. In this study, we have evaluated functional interactions between IGF- and TGF-β-regulated signaling pathways during skeletal muscle differentiation. In the mouse C2 muscle cell line and in human myoblasts in primary culture, addition of TGF-β1 blocked differentiation in a dose-dependent way, inhibited expression of muscle-specific mRNAs and proteins, and impaired myotube formation. TGF-β1 also diminished stimulation of IGF-II gene expression in myoblasts, decreased IGF-II secretion, and reduced IGF-I receptor activation. To test the hypothesis that TGF-β1 prevents muscle differentiation primarily by blocking IGF-II production, we examined effects of IGF analogues on TGF-β actions in myoblasts. Although both IGF-I and IGF-II restored muscle gene and protein expression, and stimulated myotube formation in the presence of TGF-β1, they did not reduce TGF-β1-stimulated signaling, as measured by no decline in phosphorylation of SMA and mothers against decapentaplegic homolog (Smad)3, or in induction of TGF-β-activated target genes, including a Smad-dependent promoter-reporter plasmid. Our results demonstrate that TGF-β disrupts an IGF-II-stimulated autocrine amplification cascade that is necessary for muscle differentiation in vitro. Because this inhibitory pathway can be overcome by exogenous IGFs, our observations point toward potential strategies to counteract disorders that reduce muscle mass and strength.
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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.