ArticleNature communications2017
Programmed cell senescence in skeleton during late puberty.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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
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Who cites it
59 citing papers in PubMed, 92 citations in OpenAlex.
- Divergent trajectories of structural accrual and matrix-level mechanical properties during alveolar bone maturation.Calcified tissue international · 2026Article
- Tumor cells escape from therapy-induced senescence: from molecular mechanisms to targeted intervention.Biology direct · 2026Review
- Epigenetic Targeting of Senescent Cells Prevents the Deleterious Effects of Obstructive Sleep Apnea on Growing Skeleton.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Histone modifications: Unveiling the epigenetic enigma of degenerative skeletal diseases.Journal of orthopaedic translation · 2025Review
- Pyrroloquinoline quinone targets senescent osteoclasts and reduces spinal pain and endplate degeneration in a lumbar spine instability mouse model.Journal of translational medicine · 2025Article
- The protective role of adipogenic lineage precursors in maintaining bone marrow redox homeostasis in a mouse model of prenatal dexamethasone exposure.Redox biology · 2025Article
- Stromal senescence contributes to age-related increases in cancer.Nature reviews. Cancer · 2025Review
- Unveiling the Relation between Cellular Aging, Epigenetics and Cancer.Aging and disease · 2025Article
- Scutellarin Alleviates Bone Marrow Mesenchymal Stromal Cellular Senescence via the Ezh2-Nrf2 Signalling Axis in Diabetes-Induced Bone Loss.Cell proliferation · 2025Article
- Exploring the involvement of ferroptosis-associated genes and pathways in mesenchymal stem cell aging through bioinformatics analysis.Frontiers in aging · 2025Article
- SenNet recommendations for detecting senescent cells in different tissues.Nature reviews. Molecular cell biology · 2024Review
- Genetic and Epigenetic Interactions Involved in Senescence of Stem Cells.International journal of molecular sciences · 2024Review
- Senescent-like macrophages mediate angiogenesis for endplate sclerosis via IL-10 secretion in male mice.Nature communications · 2024Article
- Diet-Stimulated Marrow Adiposity Fails to Worsen Early, Age-Related Bone Loss.Obesity facts · 2024Article
- Bone Marrow Adipose Tissue as a Critical Regulator of Postmenopausal Osteoporosis - A Concise Review.Clinical interventions in aging · 2024Review
- Significance of Premature Vertebral Mineralization in Zebrafish Models in Mechanistic and Pharmaceutical Research on Hereditary Multisystem Diseases.Biomolecules · 2023Review
- Epigenetic regulation of mesenchymal stem cell aging through histone modifications.Genes & diseases · 2023Review
- "Bone-SASP" in Skeletal Aging.Calcified tissue international · 2023Review
- Dysregulation of histone modifications in bone marrow mesenchymal stem cells during skeletal ageing: roles and therapeutic prospects.Stem cell research & therapy · 2023Review
- Development of new non-viral systems for genetic modification of senescent cells.Molecular therapy. Nucleic acids · 2023Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Mesenchymal stem/progenitor cells (MSPCs) undergo rapid self-renewal and differentiation, contributing to fast skeletal growth during childhood and puberty. It remains unclear whether these cells change their properties during late puberty to young adulthood, when bone growth and accrual decelerate. Here we show that MSPCs in primary spongiosa of long bone in mice at late puberty undergo normal programmed senescence, characterized by loss of nestin expression. MSPC senescence is epigenetically controlled by the polycomb histone methyltransferase enhancer of zeste homolog 2 (Ezh2) and its trimethylation of histone H3 on Lysine 27 (H3K27me3) mark. Ezh2 maintains the repression of key cell senescence inducer genes through H3K27me3, and deletion of Ezh2 in early pubertal mice results in premature cellular senescence, depleted MSPCs pool, and impaired osteogenesis as well as osteoporosis in later life. Our data reveals a programmed cell fate change in postnatal skeleton and unravels a regulatory mechanism underlying this phenomenon.
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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.