ArticleCell cycle (Georgetown, Tex.)2014
Geroconversion of aged muscle stem cells under regenerative pressure.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 61 citations in OpenAlex.
- The Impact of Ageing on Skeletal Muscle: Roles of Mitochondrial Dysregulation, Systemic Communication, and Exercise.Journal of cellular physiology · 2026Review
- Repair and regeneration across the lifespan: an ontogenetic perspective.Frontiers in aging · 2026Review
- The Integrated Stress Response Pathway Improves Aged Murine Muscle Stem Cell Activation andbioRxiv : the preprint server for biology · 2025Article
- Epigenetic erosion of H4K20me1 induced by inflammation drives aged stem cell ferroptosis.Nature aging · 2025Article
- Altered senescence and mitochondrial transcriptome defines age-related changes in satellite cells.Frontiers in cell and developmental biology · 2025Article
- Impact of exercise-induced DNA damage repair on age-related muscle weakness and sarcopenia.Frontiers in genetics · 2025Review
- Inflammation centered muscle signature of sarcopenia from postmenopausal women in Shanghai China.Frontiers in cell and developmental biology · 2025Article
- Semaphorins: Missing Signals in Age-dependent Alteration of Neuromuscular Junctions and Skeletal Muscle Regeneration.Aging and disease · 2024Review
- Molecular hallmarks of ageing in amyotrophic lateral sclerosis.Cellular and molecular life sciences : CMLS · 2024Review
- The Role of the Kynurenine Pathway in the Pathophysiology of Frailty, Sarcopenia, and Osteoporosis.Nutrients · 2023Review
- Article
- Cell senescence, rapamycin and hyperfunction theory of aging.Cell cycle (Georgetown, Tex.) · 2022Review
- Hallmarks of cancer and hallmarks of aging.Aging · 2022Article
- Control of satellite cell function in muscle regeneration and its disruption in ageing.Nature reviews. Molecular cell biology · 2022Review
- Current Thoughts of Notch's Role in Myoblast Regulation and Muscle-Associated Disease.International journal of environmental research and public health · 2021Review
- Anti-aging: senolytics or gerostatics (unconventional view).Oncotarget · 2021Review
- Age-related changes in polycomb gene regulation disrupt lineage fidelity in intestinal stem cells.eLife · 2021Article
- The hypothalamic-pituitary-gonadal axis controls muscle stem cell senescence through autophagosome clearance.Journal of cachexia, sarcopenia and muscle · 2021Article
- Senolytic Drugs: Reducing Senescent Cell Viability to Extend Health Span.Annual review of pharmacology and toxicology · 2021Review
- From causes of aging to death from COVID-19.Aging · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regeneration of skeletal muscle relies on a population of quiescent stem cells (satellite cells) and is impaired in very old (geriatric) individuals undergoing sarcopenia. Stem cell function is essential for organismal homeostasis, providing a renewable source of cells to repair damaged tissues. In adult organisms, age-dependent loss-of-function of tissue-specific stem cells is causally related with a decline in regenerative potential. Although environmental manipulations have shown good promise in the reversal of these conditions, recently we demonstrated that muscle stem cell aging is, in fact, a progressive process that results in persistent and irreversible changes in stem cell intrinsic properties. Global gene expression analyses uncovered an induction of p16(INK4a) in satellite cells of physiologically aged geriatric and progeric mice that inhibits satellite cell-dependent muscle regeneration. Aged satellite cells lose the repression of the INK4a locus, which switches stem cell reversible quiescence into a pre-senescent state; upon regenerative or proliferative pressure, these cells undergo accelerated senescence (geroconversion), through Rb-mediated repression of E2F target genes. p16(INK4a) silencing rejuvenated satellite cells, restoring regeneration in geriatric and progeric muscles. Thus, p16(INK4a)/Rb-driven stem cell senescence is causally implicated in the intrinsic defective regeneration of sarcopenic muscle. Here we discuss on how cellular senescence may be a common mechanism of stem cell aging at the organism level and show that induction of p16(INK4a) in young muscle stem cells through deletion of the Polycomb complex protein Bmi1 recapitulates the geriatric phenotype.
Indexed as
Identifiers
What OpenQuestion holds
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.