ReviewFrontiers in cellular neuroscience2025
Aquaporin-4 in glioblastoma: a nexus of glymphatic dysfunction, edema, immune evasion, and treatment resistance.
Review in Frontiers in cellular neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
4 citing papers in PubMed.
- Spatial organization of AQP4 water channel expression in the human brain.Science advances · 2026Article
- Glymphatic Dysfunction and Aquaporin-4 Dysregulation in Traumatic Brain Injury and Brain Tumors: A Review.Molecular neurobiology · 2026Review
- The Extracellular Matrix, the Silent 'Architect' of Glioma.Biomedicines · 2026Review
- The Glymphatic-Immune Axis in Glioblastoma: Mechanistic Insights and Translational Opportunities.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) progression is linked to aquaporin-4 (AQP4), whose functions extend beyond water transport to influence perivascular architecture, immune modulation, edema, and treatment response. In the healthy brain, AQP4 is highly polarized at astrocytic endfeet, supporting perivascular fluid exchange and glymphatic clearance. In GBM, AQP4 is frequently upregulated and mislocalized, correlating with blood-brain barrier (BBB) disruption, impaired directional fluid movement, and peritumoral edema. Peritumoral astrocytic mislocalization of AQP4, together with tumor mass effect, compromises glymphatic function by distorting perivascular spaces and compressing cerebrospinal fluid (CSF)-Interstitial fluid (ISF) exchange zones. We review evidence that AQP4 isoforms (M1 vs. M23) differentially shape motility and membrane organization, and we outline how AQP4-linked signaling axes (e.g., indoleamine 2,3-dioxygenase 1 (IDO1)/tryptophan 2,3-dioxygenase (TDO)-kynurenine-aryl hydrocarbon receptor (AhR) can bias pro-invasive states and immunosuppressive niches enriched with M2-like macrophages). We integrate a four-zone perivascular framework to localize where GBM most perturbs periarterial and perivenous pathways, as well as meningeal lymphatic outflow. Finally, we discuss therapeutic directions spanning AQP4 modulation, isoform balance, and BBB-bypassing delivery strategies. Overall, AQP4 emerges as a mechanistic hub connecting BBB instability, glymphatic impairment, edema, immune evasion, and invasion in GBM.
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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.