ArticleNature2014
Geriatric muscle stem cells switch reversible quiescence into senescence.
Article in Nature, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 586 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
586 citing papers in PubMed, 961 citations in OpenAlex.
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- From Myotubes to Skeletal Muscle:Cells · 2026Article
- Circular RNAs in Skeletal Muscle Aging and Sarcopenia: Mechanistic Evidence, Biomarker Potential, and Therapeutic Readiness.International journal of molecular sciences · 2026Review
- Review
- A compendium of circulating biomarkers of senescence in humans: Insights on mechanistic impact across health domains and modulation by therapeutic interventions.Ageing research reviews · 2026Review
- In Vitro Modeling of Sarcopenia-Related Pathology and Exercise-Associated Adaptations: Integration with In Silico Approaches.International journal of molecular sciences · 2026Review
- Metabolic Vulnerability and Regenerative Failure of the External Urethral Sphincter: A Ferroptosis-Associated Framework for Stress Urinary Incontinence.Biomolecules · 2026Review
- Integrated Transcriptomic Analysis Identifies a Candidate INHBA/Activin A-Associated Macrophage-MuSC Communication Axis in Human Skeletal Muscle Ageing.International journal of molecular sciences · 2026Article
- The hallmarks of skeletal muscle health.Nature metabolism · 2026Review
- Phase-transition failure in aged skeletal muscle regeneration.Biogerontology · 2026Review
- Rethinking Senescence Hallmarks in the Brain: Lessons From Peripheral Tissues and Challenges in Defining Neuronal Senescence.Aging cell · 2026Review
- Treating age-related loss of muscle mass and function: Where should we be focusing?The Journal of physiology · 2026Review
- Contracting myografts mimic exercise response.Nature aging · 2026Article
- State-Dependent FGF Signaling in Satellite Cell-Mediated Skeletal Muscle Regeneration and Pathological Remodeling.Biomolecules · 2026Review
- Comprehensive transcriptomic profiling reveals impaired polyamine metabolism as a contributor to age-related muscle decline.iScience · 2026Article
- Serum-induced recovery of proliferative capacity and differentiation potential in aged dental pulp stem cells.Stem cells translational medicine · 2026Article
- Epigenetic Skeletal Muscle Memory: The Impact of Physical Activity on Aging and Post-Injury Regeneration.Genes · 2026Review
- From Athletic Performance to Functional Ageing: Shared Genetic Architecture, Redox-Inflammatory Pathways and Functional Reserve Across the Life Course-A Narrative Review.Biomedicines · 2026Review
- Biomarkers and Early Mechanisms of Sarcopenia: Central Roles of Mitochondrial Dysfunction, Inflammaging, Cellular Senescence, and Neuromuscular Degeneration.International journal of molecular sciences · 2026Review
- Cellular Senescence and Aging: Mechanisms, Disease Convergence, and Therapeutic Frontiers.MedComm · 2026Review
526 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regeneration of skeletal muscle depends on a population of adult stem cells (satellite cells) that remain quiescent throughout life. Satellite cell regenerative functions decline with ageing. Here we report that geriatric satellite cells are incapable of maintaining their normal quiescent state in muscle homeostatic conditions, and that this irreversibly affects their intrinsic regenerative and self-renewal capacities. In geriatric mice, resting satellite cells lose reversible quiescence by switching to an irreversible pre-senescence state, caused by derepression of p16(INK4a) (also called Cdkn2a). On injury, these cells fail to activate and expand, undergoing accelerated entry into a full senescence state (geroconversion), even in a youthful environment. p16(INK4a) silencing in geriatric satellite cells restores quiescence and muscle regenerative functions. Our results demonstrate that maintenance of quiescence in adult life depends on the active repression of senescence pathways. As p16(INK4a) is dysregulated in human geriatric satellite cells, these findings provide the basis for stem-cell rejuvenation in sarcopenic muscles.
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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.