ArticleThe Journal of physiology2015
Genetic disruption of Smad7 impairs skeletal muscle growth and regeneration.
Article in The Journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- SMAD2 ubiquitination through PY motif regulates skeletal muscle mass and fibrotic degeneration.Scientific reports · 2026Article
- TGFβ pathway represses hepatic ribosome biogenesis and protein synthesis by regulating p70S6K-S6RP proteins.Cellular & molecular biology letters · 2026Article
- SMAD7 regulates the canonical Wnt signaling through TGF-β cascade crosstalk and SMAD7/β-CATENIN transcription factor complex formation during tooth regeneration.International journal of oral science · 2026Article
- SMAD7: riding on fibrosis-limiting routes and beyond.EMBO molecular medicine · 2025Review
- A Combination of Resveratrol and Quercetin Prevents Sarcopenic Obesity: Its Role as a Signaling Inhibitor of Myostatin/ActRIIA and ActRIIB/Smad and as an Enhancer of Insulin Actions.International journal of molecular sciences · 2025Article
- Differential regulation of MMP activity by TGFβ1 in fast- and slow- twitch muscle repair: insights from EDL and soleus muscle-derived myoblasts.Frontiers in cell and developmental biology · 2025Article
- Inhibition of miR-25 ameliorates cardiac and skeletal muscle dysfunction in agedMolecular therapy. Nucleic acids · 2024Article
- Expression profiling by high-throughput sequencing reveals GADD45, SMAD7, EGR-1 and HOXA3 activation in Myostatin (MSTN) and GDF11 treated myoblasts.Genetics and molecular biology · 2024Article
- Single-cell chromatin accessibility profiling reveals a self-renewing muscle satellite cell state.The Journal of cell biology · 2023Article
- Kinin receptors regulate skeletal muscle regeneration: differential effects for B1 and B2 receptors.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- CircCSDE1 Regulates Proliferation and Differentiation of C2C12 Myoblasts by Sponging miR-21-3p.International journal of molecular sciences · 2022Article
- Smad-dependent pathways in the infarcted and failing heart.Current opinion in pharmacology · 2022Review
- Sulforaphane Enhanced Proliferation of Porcine Satellite Cells via Epigenetic Augmentation ofAnimals : an open access journal from MDPI · 2022Article
- CaMKII oxidation is a critical performance/disease trade-off acquired at the dawn of vertebrate evolution.Nature communications · 2021Article
- Regulation of Myostatin on the Growth and Development of Skeletal Muscle.Frontiers in cell and developmental biology · 2021Review
- Article
- Smad7:β-catenin complex regulates myogenic gene transcription.Cell death & disease · 2019Article
- Micro-Ribonucleic Acid-216a Regulates Bovine Primary Muscle Cells Proliferation and DifferentiationFrontiers in genetics · 2019Article
- SMAD6 overexpression leads to accelerated myogenic differentiation of LMNA mutated cells.Scientific reports · 2018Article
- Regulation of TGF-β Family Signaling by Inhibitory Smads.Cold Spring Harbor perspectives in biology · 2017Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
key pointsSmad7 is an intracellular antagonist of transforming growth factor-β signalling pathways and modulates muscle growth in vivo. Loss of Smad7 results in decreased muscle mass, reduced force generation, fibre type switching from glycolytic towards oxidative type and delayed recovery from injury. Upregulated Smad2/3 signalling in Smad7(-/-) muscle results in reduced myoblast proliferation and differentiation. Smad7 is an important regulator of muscle growth and may be a potential intracellular therapeutic target for muscle disorders. ABSTRACT: The transforming growth factor-β (TGF-β) family of growth factors plays an essential role in mediating cellular growth and differentiation. Myostatin is a muscle-specific member of the TGF-β superfamily and a negative regulator of muscle growth. Myostatin inhibitors are currently being pursued as therapeutic options for muscle disorders. Smad7 inhibits intracellular myostatin signalling via Smad2/3, and thus presents a means of regulating myostatin and potentiating muscle growth. We investigated the functional loss of Smad7 on muscle in vivo by examining muscle growth and differentiation in mice deficient in Smad7 (Smad7(-/-) ). Smad7(-/-) mice showed reduced muscle mass, hypotrophy and hypoplasia of muscle fibres, as well as an increase in oxidative fibre types. Examination of muscle strength showed reduced force generation in vivo and ex vivo compared to wild-type controls. Analysis of muscle regeneration showed a delay in recovery, probably as a result of decreased activation, proliferation and differentiation of satellite cells, as confirmed in vitro. Additionally, myostatin expression was upregulated in Smad7(-/-) muscle. Our findings suggest that increased Smad2/3 signalling in the absence of Smad7 inhibition impedes muscle growth and regeneration. Taken together, our experiments demonstrate that Smad7 is an important mediator of muscle growth in vivo. Our studies enhance our understanding of in vivo TGF-β pathway modulation and suggest that Smad7 may be an important therapeutic target for muscle disorders.
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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.