ArticleInternational journal of molecular sciences2017
Inhibition of Aquaporin-4 Improves the Outcome of Ischaemic Stroke and Modulates Brain Paravascular Drainage Pathways.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 90 citations in OpenAlex.
- Impact of Semaglutide on Hippocampal Injury in a Streptozotocin-Induced Model of Alzheimer's Disease.Biomedicines · 2026Article
- Exploring the Therapeutic Potential of Aquaporin-4 Modulation in Sepsis: Inhibitors and Facilitators.International journal of molecular sciences · 2026Article
- Glymphatic dysfunction contributes to thalamic iron retention and secondary thalamic injury after stroke: evidence from primates and rodents.Journal of neuroinflammation · 2026Article
- Aquaporin 4 and its isoforms regulation ameliorate AQP4 Mis-localization-induced glymphatic dysfunction in ischemic stroke.Journal of advanced research · 2026Article
- Aquaporin dysfunction and impaired brain interstitial fluid clearance in Alzheimer's disease - an integrative review.Frontiers in cellular neuroscience · 2026Review
- The glymphatic system in neurodegenerative diseases and brain tumors: mechanistic insights, biomarker advances, and therapeutic opportunities.Acta neuropathologica communications · 2025Review
- Brain fluid physiology in ischaemic stroke; more than just oedema.Fluids and barriers of the CNS · 2025Review
- Aquaporins in Acute Brain Injury: Insights from Clinical and Experimental Studies.Biomedicines · 2025Review
- Aquaporin 4 modulation drives amyloid burden and cognitive abilities in an APPPS1 mouse model of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Hybrid Electro-optical Stimulation Improves Ischemic Brain Damage by Augmenting the Glymphatic System.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A novel annexin dimer targets microglial phagocytosis of astrocytes to protect the brain-blood barrier after cerebral ischemia.Acta pharmacologica Sinica · 2025Article
- Distinctive roles of aquaporins and novel therapeutic opportunities against cancer.RSC medicinal chemistry · 2025Review
- Glymphatic system: a self-purification circulation in brain.Frontiers in cellular neuroscience · 2025Review
- Channels and Transporters in Ischemic Brain Edema.Journal of inflammation research · 2025Review
- Formaldehyde initiates memory and motor impairments under weightlessness condition.NPJ microgravity · 2024Review
- Non-coding RNAs and Aquaporin 4: Their Role in the Pathogenesis of Neurological Disorders.Neurochemical research · 2024Review
- Review
- Glymphatic and lymphatic communication with systemic responses during physiological and pathological conditions in the central nervous system.Communications biology · 2024Review
- TGN-020 Alleviate Inflammation and Apoptosis After Cerebral Ischemia-Reperfusion Injury in Mice Through Glymphatic and ERK1/2 Signaling Pathway.Molecular neurobiology · 2024Article
- Astrocyte regulation of extracellular space parameters across the sleep-wake cycle.Frontiers in cellular neuroscience · 2024Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aquaporin-4 (AQP4) is the most abundant water channel in the brain, and its inhibition before inducing focal ischemia, using the AQP4 inhibitor TGN-020, has been showed to reduce oedema in imaging studies. Here, we aimed to evaluate, for the first time, the histopathological effects of a single dose of TGN-020 administered after the occlusion of the medial cerebral artery (MCAO). On a rat model of non-reperfusion ischemia, we have assessed vascular densities, albumin extravasation, gliosis, and apoptosis at 3 and 7 days after MCAO. TGN-020 significantly reduced oedema, glial scar, albumin effusion, and apoptosis, at both 3 and 7 days after MCAO. The area of GFAP-positive gliotic rim decreased, and 3D fractal analysis of astrocytic processes revealed a less complex architecture, possibly indicating water accumulating in the cytoplasm. Evaluation of the blood vessels revealed thicker basement membranes colocalizing with exudated albumin in the treated animals, suggesting that inhibition of AQP4 blocks fluid flow towards the parenchyma in the paravascular drainage pathways of the interstitial fluid. These findings suggest that a single dose of an AQP4 inhibitor can reduce brain oedema, even if administered after the onset of ischemia, and AQP4 agonists/antagonists might be effective modulators of the paravascular drainage flow.
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