ArticleNeuro-oncology2023
Inhibition of integrated stress response protects against lipid-induced senescence in hypothalamic neural stem cells in adamantinomatous craniopharyngioma.
Article in Neuro-oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The oxytocin system in patients with craniopharyngioma: A systematic review.Frontiers in neuroendocrinology · 2025Pooled it
- Exploring molecular signatures of senescence with marker, an R Toolkit for evaluating gene sets as phenotypic markers.NAR genomics and bioinformatics · 2026Article
- The role of lipid metabolism in neuronal senescence.FEBS open bio · 2026Review
- A Patient-Derived Organoid Biobank of Adamantinomatous Craniopharyngioma as a Platform for Drug Discovery.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Modulating Macrophage-Nucleus Pulposus Cell Crosstalk via Sequential Drug Delivery Attenuates Disc Degeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Oxytocin System and Implications for Oxytocin Deficiency in Hypothalamic-Pituitary Disease.Endocrine reviews · 2025Review
- ATP11B Modulates Microglial Lipid Metabolism and Alleviates Alzheimer's Disease Pathology.MedComm · 2025Article
- Anlotinib may have a therapeutic effect on papillary craniopharyngiomas without the BRAFv600e mutation.Acta neuropathologica communications · 2025Article
- Characteristics of the blood-brain barrier in pediatric brain tumors.Frontiers in pediatrics · 2025Review
- Differential proteomic profiles of exosomes in pediatric and adult adamantinomatous craniopharyngioma cyst fluid.Molecular biology reports · 2024Article
- Unraveling the complexity of the senescence-associated secretory phenotype in adamantinomatous craniopharyngioma using multimodal machine learning analysis.Neuro-oncology · 2024Article
- A New Insight into the Mechanism of Atrazine-Induced Neurotoxicity: Triggering Neural Stem Cell Senescence by Activating the Integrated Stress Response Pathway.Research (Washington, D.C.) · 2024Article
- Integrated Stress Response (ISR) Pathway: Unraveling Its Role in Cellular Senescence.International journal of molecular sciences · 2023Review
- Emergence of Lipid Droplets in the Mechanisms of Carcinogenesis and Therapeutic Responses.Cancers · 2023Review
- A promising future for hypothalamic dysfunction in craniopharyngioma.Neuro-oncology · 2023Article
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17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAdamantinomatous craniopharyngioma (ACP) is a benign tumor with malignant clinical manifestations. ACP adjacent to the hypothalamus often presents with more severe symptoms and higher incidence of hypothalamic dysfunction. However, the mechanism underlying hypothalamic dysfunction remains unclear.
methodsImmunostaining was performed to determine the nerve damage to the floor of the third ventricle (3VF) adjacent to ACP and to examine the recruitment and senescence of hypothalamic neural stem cells (htNSCs). The accumulation of lipid droplets (LDs) in htNSCs was evaluated via BODIPY staining, oil red O staining, and transmission electron microscopy. In vitro and in vivo assays were used to evaluate the effect of cystic fluid or oxidized low-density lipoprotein and that of oxytocin (OXT) on htNSC senescence and the hypothalamic function. The protein expression levels were analyzed using western blotting.
resultshtNSCs with massive LD accumulation were recruited to the damaged 3VF adjacent to ACP. The LDs in htNSCs induced senescence and reduced neuronal differentiation; however, htNSC senescence was effectively prevented by inhibiting either CD36 or integrated stress response (ISR) signaling. Furthermore, OXT pretreatment reduced lipotoxicity via the inhibition of ISR signaling and the repair of the blood-brain barrier.
conclusionsReduced LD aggregation or ISR signaling inhibition prevented senescence in htNSCs and identified molecular pathways and potential therapeutic targets that may improve hypothalamic dysfunction in ACP patients.
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