ArticleNature communications2013
Normal muscle regeneration requires tight control of muscle cell fusion by tetraspanins CD9 and CD81.
Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 110 citations in OpenAlex.
- Extracellular vesicle transcriptomic analysis to investigate muscle adaptation in microgravity.iScience · 2026Article
- Building the bridges: molecular mechanisms of tunneling nanotube formation.Cellular and molecular life sciences : CMLS · 2026Review
- PDGFRβ signaling restrains myocyte function to limit the regenerative capacity of skeletal muscle.The Journal of clinical investigation · 2026Article
- Review
- Quantitative 3D assessment of muscle dystrophy through X-ray phase-contrast tomography.Scientific reports · 2025Article
- Mapping the placental galectin-3 interactome identifies CD9 and ITGB1 as functional glycoprotein counterreceptors during syncytialization.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Tuberculosis Patients' Serum Extracellular Vesicles Induce Relevant Immune Responses for Initial Defense Against BCG in Mice.Microorganisms · 2025Article
- Review
- Suppressing PDGFRβ Signaling Enhances Myocyte Fusion to Promote Skeletal Muscle Regeneration.bioRxiv : the preprint server for biology · 2024Article
- Proteomic landscape of tunneling nanotubes reveals CD9 and CD81 tetraspanins as key regulators.eLife · 2024Article
- Tetraspanin proteins in membrane remodeling processes.Journal of cell science · 2024Review
- Three-dimensional imaging studies in mice identify cellular dynamics of skeletal muscle regeneration.Developmental cell · 2024Article
- Smart exosomes enhance PDAC targeted therapy.Journal of controlled release : official journal of the Controlled Release Society · 2024Article
- Targeting of Tetraspanin CD81 with Monoclonal Antibodies and Small Molecules to Combat Cancers and Viral Diseases.Cancers · 2023Review
- Extracellular vesicle distribution and localization in skeletal muscle at rest and following disuse atrophy.Skeletal muscle · 2023Article
- Prognostic value and multifaceted roles of tetraspanin CD9 in cancer.Frontiers in oncology · 2023Review
- Juvenile zebrafish (Danio rerio) are able to recover from lordosis.Scientific reports · 2022Article
- Integrative analysis of cell adhesion molecules in glioblastoma identified prostaglandin F2 receptor inhibitor (PTGFRN) as an essential gene.BMC cancer · 2022Review
- The metalloprotease ADM-4/ADAM17 promotes axonal repair.Science advances · 2022Article
- Cell Surface Proteins for Enrichment andStem cells international · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle regeneration after injury follows a remarkable sequence of synchronized events. However, the mechanisms regulating the typical organization of the regenerating muscle at different stages remain largely unknown. Here we show that muscle regeneration in mice lacking either CD9 or CD81 is abnormal and characterized by the formation of discrete giant dystrophic myofibres, which form more quickly in the absence of both tetraspanins. We also show that, in myoblasts, these two tetraspanins associate with the immunoglobulin domain molecule CD9P-1 (EWI-F/FPRP), and that grafting of CD9P-1-depleted myoblasts in regenerating muscles also leads to abnormal regeneration. In vitro myotubes lacking CD9P-1 or both CD9 and CD81 fuse with a higher frequency than normal myotubes. Our study unveils a mechanism preventing inappropriate fusion of myotubes that has an important role in the restitution of normal muscle architecture during 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.