ArticleJCI insight2024
All-trans retinoic acid inhibits glioblastoma progression and attenuates radiation-induced brain injury.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Paeoniflorin Attenuates Radiation-Induced Brain Injury Associated with Modulation of Microglial Polarization and ERK/MAPK Signaling.ACS omega · 2026Article
- Isoliquiritigenin, a Bioactive Blood Component Derived from Licorice, Activates Nrf2 Enzymes to Confer Protection Against Radiation-Induced Nerve Injury.Antioxidants (Basel, Switzerland) · 2026Article
- Single-cell sequencing analysis and machine learning model reveal aberrant TIM-3 expression in microglia during Alzheimer's disease progression.Journal of translational medicine · 2026Article
- Significance of Vitamins A and E in Cancer Progression and Prevention.International journal of molecular sciences · 2025Review
- Spatial transcriptomics of glioblastoma defines biologically and clinically significant reprogramming patterns across unique spatial microenvironments.bioRxiv : the preprint server for biology · 2025Article
- Urolithin A in Central Nervous System Disorders: Therapeutic Applications and Challenges.Biomedicines · 2025Review
- Drug protection against radiation-induced neurological injury: mechanisms and developments.Archives of toxicology · 2025Review
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radiotherapy (RT) remains a primary treatment modality for glioblastoma (GBM), but it induces cellular senescence and is strongly implicated in GBM progression and RT-related injury. Recently, eliminating senescent cells has emerged as a promising strategy for treating cancer and for mitigating radiation-induced brain injury (RBI). Here, we investigated the impact of all-trans retinoic acid (RA) on radiation-induced senescence. The findings of this study revealed that RA effectively eliminated astrocytes, which are particularly prone to senescence after radiation, and that the removal of senescence-associated secretory phenotype factor-producing astrocytes inhibited GBM cell proliferation in vitro. Moreover, RA-mediated clearance of senescent cells improved survival in GBM-bearing mice and alleviated radiation-induced cognitive impairment. Through RNA sequencing, we found that the AKT/mTOR/PPARγ/Plin4 signaling pathway is involved in RA-mediated clearance of senescent cells. In summary, these results suggest that RA could be a potential senolytic drug for preventing GBM progression and improving RBI.
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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.