ArticleNeuro-oncology2019
Radiation-induced astrocyte senescence is rescued by Δ133p53.
Article in Neuro-oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.
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Who cites it
85 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.
- Does protracted radon exposure play a role in the development of dementia?Environmental research · 2022Pooled it
- Loss of killifish cGAS attenuates age-related signatures but does not affect organismal life span.EMBO reports · 2026Article
- Updated Knowledge on Radon Exposure: Quantification Methods, Health Effects, and Molecular Mechanisms.Environment & health (Washington, D.C.) · 2026Review
- The p53 Isoforms as Potential Biomarkers in Different Cancer Entities.International journal of molecular sciences · 2026Review
- The senescence-inhibitory p53 isoform Δ133p53α: enhancing cancer immunotherapy and exploring novel therapeutic approaches for senescence-associated diseases.GeroScience · 2026Review
- Senescence-inhibitory Δ133p53α counteracts accelerated ageing and mortality.bioRxiv : the preprint server for biology · 2026Article
- Senescent Astrocytes: A New Player in Brain Aging and Cognitive Decline.Brain sciences · 2026Review
- The Implications of Radiotherapy-Induced Cellular Senescence for Cancer Treatment and Tumor Microenvironment Modulation.International journal of biological sciences · 2026Review
- Late radiation necrosis following stereotactic radiosurgery after COVID-19 vaccination: a case report and hypothesis of immune-mediated inflammatory activation.Frontiers in oncology · 2026Article
- Navitoclax acts synergistically with irradiation to induce apoptosis in preclinical models of H3K27M-altered diffuse midline glioma.Scientific reports · 2025Article
- Review
- Cranial radiotherapy profoundly affects glia without inducing widespread cellular senescence.Neuro-oncology · 2025Article
- Radiation-induced Brain Injury and the Radiation Late Effects Cohort (RLEC) of Rhesus Macaques (Macaca mulatta).Radiation research · 2025Review
- A Murine Model of Glioblastoma Initiating Cells and Human Brain Organoid Xenograft for Photodynamic Therapy Testing.International journal of molecular sciences · 2025Article
- Δ133p53α-mediated inhibition of astrocyte senescence and neurotoxicity as a possible therapeutic approach for neurodegenerative diseases.Neuroscience · 2025Review
- A Quantitative High-Throughput Screen Identifies Compounds that Upregulate the p53 Isoform Δ133p53α and Inhibit Cellular Senescence.ACS pharmacology & translational science · 2025Article
- Central Nervous System Response Against Ionizing Radiation Exposure: Cellular, Biochemical, and Molecular Perspectives.Molecular neurobiology · 2025Review
- Distinct astrocyte activation patterns associated with neuroinflammation induced by gamma and proton beam irradiation.Scientific reports · 2025Article
- Drug protection against radiation-induced neurological injury: mechanisms and developments.Archives of toxicology · 2025Review
- Crosstalk between neuroinflammation and ferroptosis: Implications for Parkinson's disease progression.Frontiers in pharmacology · 2025Review
25 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
13 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundCellular senescence and the senescence-associated secretory phenotype (SASP) may contribute to the development of radiation therapy-associated side effects in the lung and blood vessels by promoting chronic inflammation. In the brain, inflammation contributes to the development of neurologic disease, including Alzheimer's disease. In this study, we investigated the roles of cellular senescence and Δ133p53, an inhibitory isoform of p53, in radiation-induced brain injury.
methodsSenescent cell types in irradiated human brain were identified with immunohistochemical labeling of senescence-associated proteins p16INK4A and heterochromatin protein Hp1γ in 13 patient cases, including 7 irradiated samples. To investigate the impact of radiation on astrocytes specifically, primary human astrocytes were irradiated and examined for expression of Δ133p53 and induction of SASP. Lentiviral expression of ∆133p53 was performed to investigate its role in regulating radiation-induced cellular senescence and astrocyte-mediated neuroinflammation.
resultsAstrocytes expressing p16INK4A and Hp1γ were identified in all irradiated tissues, were increased in number in irradiated compared with untreated cancer patient tissues, and had higher labeling intensity in irradiated tissues compared with age-matched controls. Human astrocytes irradiated in vitro also experience induction of cellular senescence, have diminished Δ133p53, and adopt a neurotoxic phenotype as demonstrated by increased senescence-associated beta-galactosidase activity, p16INK4A, and interleukin (IL)-6. In human astrocytes, Δ133p53 inhibits radiation-induced senescence, promotes DNA double-strand break repair, and prevents astrocyte-mediated neuroinflammation and neurotoxicity.
conclusionsRestoring expression of the endogenous p53 isoform, ∆133p53, protects astrocytes from radiation-induced senescence, promotes DNA repair, and inhibits astrocyte-mediated neuroinflammation.
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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.