From:  The role of the glymphatic system in cerebral ischemia: pathological implications and future perspectives

 Experimental evidence on the role of AQP-4 in cerebral ischemia and edema.

Study/AuthorModelInterventionMain findingsClinical implication
Kato et al. [43]Cerebral infarction in miceObservation of AQP-4 localizationAQP-4 shifts from perivascular end-feet to astrocytic soma; it reduces metabolite and cytokine clearance.Loss of AQP-4 polarity worsens inflammation and neuronal damage. However, being an observational study, it does not provide direct evidence on therapeutic interventions.
Yang et al. [5]Cerebral ischemia in miceDP71 analysisDP71 stabilizes AQP-4 anchorage; its degradation alters localization and outflow.DP71 as a potential therapeutic target. Provides mechanistic insight into scaffolding proteins regulating AQP-4. Suggests that protecting DP71 could indirectly preserve glymphatic flow.
Mestre et al. [38]MCA occlusion in miceAQP-4 knockoutNo cerebral edema in the first 15 min.AQP-4 is essential for early cytotoxic edema. Reinforces the importance of timing: benefits are evident only in acute stages.
Li et al. [44]Ischemia-reperfusion in miceTGN-020Reduces inflammation and apoptosis via GS and ERK1/2.AQP-4 inhibition may modulate neuroinflammation.
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AQP-4: aquaporin-4; DP71: dystrophin-71; MCA: middle cerebral artery; TGN-020: N-(1,3,4-thiadiazol-2-yl) pyridine-3-carboxamide dihydrochloride.