ArticleNature communications2015
Numb is required to prevent p53-dependent senescence following skeletal muscle injury.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
What it found
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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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- A systematic review of p53 regulation of oxidative stress in skeletal muscle.Redox report : communications in free radical research · 2018Pooled it
- GDF5 modulation of MuSC pool as a potential therapeutic benefit for DMD.Molecular therapy. Nucleic acids · 2026Article
- LaminA/C-dependent cellular senescence signaling promotes skeletal muscle atrophy and abnormalities in Parkinson's disease.Cell death & disease · 2026Article
- Cellular senescence in skeletal muscle regeneration.Cell regeneration (London, England) · 2026Review
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- Cellular senescence in musculoskeletal diseases: biological mechanisms and clinical implications.Theranostics · 2026Review
- Non-canonical roles of Keap1/Nrf2 in regulating quiescence and early activation in adult muscle stem cells.Nature communications · 2025Article
- Revolutionizing Diabetic Foot Ulcer Care: The Senotherapeutic Approach.Aging and disease · 2024Review
- Cellular senescence contributes to mechanical ventilation-induced diaphragm dysfunction by upregulating p53 signalling pathways.BMC pulmonary medicine · 2023Article
- Senescent cells enhance newt limb regeneration by promoting muscle dedifferentiation.Aging cell · 2023Article
- Cellular senescence in malignant cells promotes tumor progression in mouse and patient Glioblastoma.Nature communications · 2023Article
- Notch, Numb and Numb-like responses to exercise-induced muscle damage in human skeletal muscle.Experimental physiology · 2022Article
- Endogenous expression of Notch pathway molecules in human trabecular meshwork cells.Experimental eye research · 2022Article
- A Long Journey before Cycling: Regulation of Quiescence Exit in Adult Muscle Satellite Cells.International journal of molecular sciences · 2022Review
- p53 convergently activates Dux/DUX4 in embryonic stem cells and in facioscapulohumeral muscular dystrophy cell models.Nature genetics · 2021Article
- Paxbp1 controls a key checkpoint for cell growth and survival during early activation of quiescent muscle satellite cells.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- From Development to Aging: The Path to Cellular Senescence.Antioxidants & redox signaling · 2021Review
- Diverse Roles of Cellular Senescence in Skeletal Muscle Inflammation, Regeneration, and Therapeutics.Frontiers in pharmacology · 2021Review
- Senescent cells and macrophages: key players for regeneration?Open biology · 2020Review
- Satellite cell-specific ablation of Cdon impairs integrin activation, FGF signalling, and muscle regeneration.Journal of cachexia, sarcopenia and muscle · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Regeneration relies on coordinated action of multiple cell types to reconstitute the damaged tissue. Here we inactivate the endocytic adaptor protein Numb in skeletal muscle stem cells prior to chronic or severe muscle injury in mice. We observe two types of senescence in regenerating muscle; a transient senescence in non-myogenic cells of control and Numb mutant mice that partly depends on INK4a/ARF activity, and a persistent senescence in myogenic cells lacking Numb. The senescence levels of Numb-deficient muscle is reduced to wild type levels by an anti-oxidant treatment or p53 ablation, resulting in functional rescue of the regenerative potential in Numb mutants. Ex vivo experiments suggest that Numb-deficient senescent cells recruit macrophages to sustain inflammation and drive fibrosis, two hallmarks of the impaired muscle regeneration in Numb mutants. These findings provide insights into previously reported developmental and oncogenic senescence that are also differentially regulated by p53.
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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.