ArticleAging cell2017
DNA damage and senescence in osteoprogenitors expressing Osx1 may cause their decrease with age.
Article in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
110 citing papers in PubMed, 1 synthesis or guideline pooled it, 184 citations in OpenAlex.
- Consequences of Aging on Bone.Aging and disease · 2023Pooled it
- Cellular senescence and the SASP in skeletal ageing: convergent mechanisms of progressive bone loss in osteoporosis.Biogerontology · 2026Review
- The vicious cycle of SASP and inflammaging promotes aging and age-related diseases.Communications biology · 2026Review
- Cellular Senescence and Aging: Mechanisms, Disease Convergence, and Therapeutic Frontiers.MedComm · 2026Review
- Mechanisms limiting the long-term anabolic effects of teriparatide (PTH 1-34) on bone.JBMR plus · 2026Review
- Overview of molecular signatures of senescence and associated resources: pros and cons.FEBS open bio · 2026Review
- Cellular senescence in musculoskeletal diseases: biological mechanisms and clinical implications.Theranostics · 2026Review
- Osteoimmune senescence in aging bone: from inflammaging dogma to cell-type-specific therapeutic windows.Frontiers in immunology · 2026Review
- Article
- Lipid-Driven Immunometabolism in Mesenchymal Stromal Cells: A New Axis for Musculoskeletal Regeneration.International journal of molecular sciences · 2025Review
- Targeting Cellular Senescence: Pathophysiology in Multisystem Age-Related Diseases.Biomedicines · 2025Review
- Addressing osteoblast senescence: Molecular pathways and the frontier of anti-ageing treatments.Clinical and translational medicine · 2025Review
- CCN Proteins as Matricellular Regulators of Bone in Aging and Disease.Current osteoporosis reports · 2025Review
- The adverse effects of chemotherapy on bone mass are not prevented by senolytics.Scientific reports · 2025Article
- Insights into age-related osteoporosis from senescence-based preclinical models and human accelerated aging paradigms.Mechanisms of ageing and development · 2025Review
- Skeletal stem and progenitor cells in bone physiology, ageing and disease.Nature reviews. Endocrinology · 2025Review
- 3D imaging reveals changes in the neurovascular architecture of the murine calvarium with aging.Bone research · 2025Article
- Deletion of the scavenger receptor Scarb1 in osteoblast progenitors and myeloid cells does not affect bone mass.PloS one · 2025Article
- Oligomeric Proanthocyanidins Ameliorate Cadmium-Induced Senescence of Osteocytes Through Combating Oxidative Stress and Inflammation.Antioxidants (Basel, Switzerland) · 2024Article
- Ageing-related bone and immunity changes: insights into the complex interplay between the skeleton and the immune system.Bone research · 2024Review
50 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Age-related bone loss in mice results from a decrease in bone formation and an increase in cortical bone resorption. The former is accounted by a decrease in the number of postmitotic osteoblasts which synthesize the bone matrix and is thought to be the consequence of age-dependent changes in mesenchymal osteoblast progenitors. However, there are no specific markers for these progenitors, and conclusions rely on results from in vitro cultures of mixed cell populations. Moreover, the culprits of such changes remain unknown. Here, we have used Osx1-Cre;TdRFP mice in which osteoprogenitors express the TdRFP fluorescent protein. We report that the number of TdRFP-Osx1 cells, freshly isolated from the bone marrow, declines by more than 50% between 6 and 24 months of age in both female and male mice. Moreover, TdRFP-Osx1 cells from old mice exhibited markers of DNA damage and senescence, such as γH2AX foci, G1 cell cycle arrest, phosphorylation of p53, increased p21
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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.