ArticlePloS one2013
Loss of the osteogenic differentiation potential during senescence is limited to bone progenitor cells and is dependent on p53.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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
30 citing papers in PubMed.
- Review
- Autophagy: regulating the seesaw of bone-fat balance.Frontiers in cell and developmental biology · 2025Review
- Advancements in extracellular vesicle targeted therapies for rheumatoid arthritis: insights into cellular origins, current perspectives, and emerging challenges.Stem cell research & therapy · 2024Review
- Senescence during early differentiation reduced the chondrogenic differentiation capacity of mesenchymal progenitor cells.Frontiers in bioengineering and biotechnology · 2023Article
- Annexin A2 Improves the Osteogenic Differentiation of Mesenchymal Stem Cells Exposed to High-Glucose Conditions through Lessening the Senescence.International journal of molecular sciences · 2022Article
- Does Aging Activate T-cells to Reduce Bone Mass and Quality?Current osteoporosis reports · 2022Review
- Artificial Mitochondrial Transfer (AMT) for the Management of Age-related Musculoskeletal Degenerative Disorders: An Emerging Avenue for Bone and Cartilage Metabolism Regulation.Stem cell reviews and reports · 2022Article
- Article
- Identification of Molecules Responsible for Therapeutic Effects of Extracellular Vesicles Produced from iPSC-Derived MSCs on Sjo¨gren's Syndrome.Aging and disease · 2021Article
- In search of elixir: Pharmacological agents against stem cell senescence.Iranian journal of basic medical sciences · 2021Review
- Bone Aging, Cellular Senescence, and Osteoporosis.JBMR plus · 2021Review
- Effects of Cellular Senescence on Dental Follicle Cells.Pharmacology · 2021Review
- Comprehensive Molecular Profiles of Functionally Effective MSC-Derived Extracellular Vesicles in Immunomodulation.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Augmentation of Bone Regeneration by Depletion of Stress-Induced Senescent Cells Using Catechin and Senolytics.International journal of molecular sciences · 2020Article
- Looking for immortality: Review of phytotherapy for stem cell senescence.Iranian journal of basic medical sciences · 2020Review
- The Role of Mesenchymal Stem Cells in Radiation-Induced Lung Fibrosis.International journal of molecular sciences · 2019Review
- Article
- Single-Cell Transcriptomics of Human Mesenchymal Stem Cells Reveal Age-Related Cellular Subpopulation Depletion and Impaired Regenerative Function.Stem cells (Dayton, Ohio) · 2019Article
- Silk Biomaterials-Mediated miRNA Functionalized Orthopedic Devices.Tissue engineering. Part A · 2019Article
- INK4a/ARF Expression Impairs Neurogenesis in the Brain of Irradiated Mice.Stem cell reports · 2018Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
DNA damage can lead to the induction of cellular senescence. In particular, we showed that exposure to ionizing radiation (IR) leads to the senescence of bone marrow-derived multipotent stromal cells (MSC) and osteoblast-like stromal cells (OB-SC), a phenotype associated with bone loss. The mechanism by which IR leads to bone dysfunction is not fully understood. One possibility involves that DNA damage-induced senescence limits the regeneration of bone progenitor cells. Another possibility entails that bone dysfunction arises from the inability of accumulating senescent cells to fulfill their physiological function. Indeed, we show here that exposure to IR prevented the differentiation and mineralization functions of MSC, an effect we found was limited to this population as more differentiated OB-SC could still form mineralize nodules. This is in contrast to adipogenesis, which was inhibited in both IR-induced senescent MSC and 3T3-L1 pre-adipocytes. Furthermore, we demonstrate that IR-induced loss of osteogenic potential in MSC was p53-dependent, a phenotype that correlates with the inability to upregulate key osteogenic transcription factors. These results are the first to demonstrate that senescence impacts osteogenesis in a cell type dependent manner and suggest that the accumulation of senescent osteoblasts is unlikely to significantly contribute to bone dysfunction in a cell autonomous manner.
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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.