ArticleCell research2011
Smad3 signaling is required for satellite cell function and myogenic differentiation of myoblasts.
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 54 papers, 1 of them a synthesis that pooled it.
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Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.
- Multi-ancestry genome-wide association study of serum creatine kinase implicates myopathy genes and muscle pathways.EBioMedicine · 2026Pooled it
- BetaThe Journal of physiology · 2018Trial
- Myostatin Orchestrates miR-124-Mediated Epigenetic Silencing ofBiomolecules · 2026Article
- Targeting muscle wasting: Bioinformatics-derived ubiquitination genes as potential therapeutic targets for sarcopenia.Medicine · 2026Article
- Downregulated Smad3 signaling impairs the maturation of MO-MDSC in colorectal cancer.Cell death & disease · 2025Article
- TGFβ-Smad3 signaling restores cell-autonomous Srsf1-mediated splicing of fibronectin in aged skeletal muscle stem cells.Nature communications · 2025Article
- Pretreatment of Mice with 830 nm Light Enhances Endurance During Acute Exercise.Muscles (Basel, Switzerland) · 2025Article
- Transcriptional regulation of autophagy in skeletal muscle stem cells.Disease models & mechanisms · 2025Review
- Reduced myotube diameter induced by combined inhibition of transforming growth factor-β type I receptors Acvr1b and Tgfbr1 is associated with enhanced β1-syntrophin expression.Journal of cellular physiology · 2024Article
- SPSB1-mediated inhibition of TGF-β receptor-II impairs myogenesis in inflammation.Journal of cachexia, sarcopenia and muscle · 2023Article
- Article
- Multiscale 3D genome reorganization during skeletal muscle stem cell lineage progression and aging.Science advances · 2023Article
- Enhanced Muscle Fibers ofInternational journal of molecular sciences · 2022Article
- Myostatin/Activin Receptor Ligands in Muscle and the Development Status of Attenuating Drugs.Endocrine reviews · 2022Review
- Can Exercise Training Alter Human Skeletal Muscle DNA Methylation?Metabolites · 2022Article
- Peripheral blood mononuclear cells contribute to myogenesis in a 3D bioengineered system of bone marrow mesenchymal stem cells and myoblasts.Frontiers in bioengineering and biotechnology · 2022Article
- Inhibition ofFrontiers in cell and developmental biology · 2021Article
- Article
- Peptidyl-prolyl cis-trans isomerase NIMA interacting 1 regulates skeletal muscle fusion through structural modification of Smad3 in the linker region.Journal of cellular physiology · 2018Article
- All-trans retinoic acid increases the expression of oxidative myosin heavy chain through the PPARδ pathway in bovine muscle cells derived from satellite cells.Journal of animal science · 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
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TGF-β and myostatin are the two most important regulators of muscle growth. Both growth factors have been shown to signal through a Smad3-dependent pathway. However to date, the role of Smad3 in muscle growth and differentiation is not investigated. Here, we demonstrate that Smad3-null mice have decreased muscle mass and pronounced skeletal muscle atrophy. Consistent with this, we also find increased protein ubiquitination and elevated levels of the ubiquitin E3 ligase MuRF1 in muscle tissue isolated from Smad3-null mice. Loss of Smad3 also led to defective satellite cell (SC) functionality. Smad3-null SCs showed reduced propensity for self-renewal, which may lead to a progressive loss of SC number. Indeed, decreased SC number was observed in skeletal muscle from Smad3-null mice showing signs of severe muscle wasting. Further in vitro analysis of primary myoblast cultures identified that Smad3-null myoblasts exhibit impaired proliferation, differentiation and fusion, resulting in the formation of atrophied myotubes. A search for the molecular mechanism revealed that loss of Smad3 results in increased myostatin expression in Smad3-null muscle and myoblasts. Given that myostatin is a negative regulator, we hypothesize that increased myostatin levels are responsible for the atrophic phenotype in Smad3-null mice. Consistent with this theory, inactivation of myostatin in Smad3-null mice rescues the muscle atrophy phenotype.
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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.