ArticleNeuro-oncology2024
Defective autophagy of pericytes enhances radiation-induced senescence promoting radiation brain injury.
Article in Neuro-oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.
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Who cites it
25 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Surgical management of pediatric pineal region tumors: an overview of current strategies.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2026Pooled it
- Surgical management of pineal region tumors in Italy: a SINch (SINch®) National Survey with systematic review.Neurosurgical review · 2026Pooled it
- Cellular senescence and regulated cell death in cancer: mechanisms, cross-regulatory networks and therapeutic implications.Journal of hematology & oncology · 2026Review
- LINP1 suppresses radiation-induced cellular senescence in keratinocytes by modulating the mTOR-p53 axis.Molecular and cellular biochemistry · 2026Article
- Radiotherapy and cytokines: A systems view of immunotherapy and toxicity (Review).International journal of molecular medicine · 2026Review
- Single-Nucleus Profiling Reveals a BBB Senescence Unit Driving AD Pathology in Human Brain.Molecular neurobiology · 2026Article
- Isoliquiritigenin, a Bioactive Blood Component Derived from Licorice, Activates Nrf2 Enzymes to Confer Protection Against Radiation-Induced Nerve Injury.Antioxidants (Basel, Switzerland) · 2026Article
- Ergothioneine attenuates whole-abdominal irradiation-induced multi-organ injury via the gut-heart-brain axis by modulating calcium voltage-gated channel subunit alpha1 C (Cacna1c) expression.Molecular biomedicine · 2026Article
- Metformin and butyrate attenuate chronic radiation proctitis by alleviating inflammation and macrophage senescence.Frontiers in immunology · 2026Article
- Decoding autophagy in neuro-tumor crosstalk: from underlying mechanisms to translational opportunities.Theranostics · 2026Review
- A review of neuroprotective properties ofAnnals of medicine · 2025Review
- Cytokine CCL2 secreted by cancer-associated fibroblasts augments temozolomide resistance in glioblastoma through ERK1/2 signaling.Oncogene · 2025Article
- Targeting gut microbiota and metabolites in cancer radiotherapy.Clinical and translational medicine · 2025Review
- Robotic surgery in healthcare: current challenges, technological advances, and global implementation prospects.Journal of robotic surgery · 2025Review
- Cellular senescence in cancer: from mechanism paradoxes to precision therapeutics.Molecular cancer · 2025Review
- Radiation Exposure Induced Blood-Brain Barrier Injury via Mitochondria-Mediated Sterile Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Aging microvasculature: Effects on immune cell trafficking and inflammatory diseases.The Journal of experimental medicine · 2025Review
- Urolithin A in Central Nervous System Disorders: Therapeutic Applications and Challenges.Biomedicines · 2025Review
- Mechanisms of endothelial senescence and vascular aging.Biogerontology · 2025Review
- Autophagy mediated immune response regulation and drug resistance in cancer.Molecular biology reports · 2025Review
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
backgroundRadiation-induced brain injury (RBI) represents a major challenge for cancer patients undergoing cranial radiotherapy. However, the molecular mechanisms and therapeutic strategies of RBI remain inconclusive. With the continuous exploration of the mechanisms of RBI, an increasing number of studies have implicated cerebrovascular dysfunction as a key factor in RBI-related cognitive impairment. As pericytes are a component of the neurovascular unit, there is still a lack of understanding in current research about the specific role and function of pericytes in RBI.
methodsWe constructed a mouse model of RBI-associated cognitive dysfunction in vivo and an in vitro radiation-induced pericyte model to explore the effects of senescent pericytes on the blood-brain barrier (BBB) and normal central nervous system cells, even glioma cells. To further clarify the effects of pericyte autophagy on senescence, molecular mechanisms were explored at the animal and cellular levels. Finally, we validated the clearance of pericyte senescence by using a senolytic drug and all-trans retinoic acid to investigate the role of radiation-induced pericyte senescence.
resultsOur findings indicated that radiation-induced pericyte senescence plays a key role in BBB dysfunction, leading to RBI and subsequent cognitive decline. Strikingly, pericyte senescence also contributed to the growth and invasion of glioma cells. We further demonstrated that defective autophagy in pericytes is a vital regulatory mechanism for pericyte senescence. Moreover, autophagy activated by rapamycin could reverse pericyte senescence. Notably, the elimination of senescent cells by senolytic drugs significantly mitigated radiation-induced cognitive dysfunction.
conclusionsOur results demonstrated that pericyte senescence may be a promising therapeutic target for RBI and glioma progression.
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