ArticleFrontiers in immunology2026
Aquaporin-4 suppresses neuronal pyroptosis after ischemic stroke via the IκBα/NF-κB signaling pathway.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Ischemic stroke, a predominant cause of global mortality and disability, involves complex pathophysiological processes where neuroinflammation and pyroptosis play a crucial role. We aimed to investigate the role of the brain's major water channel Aquaporin-4 (AQP4) in regulating neuronal pyroptosis, a highly inflammatory form of cell death, following cerebral ischemia. Methods: Utilizing integrated Results: Our results demonstrated that AQP4 deficiency significantly worsened neurological deficits, enlarged infarct volume, and intensified oxidative stress. Crucially, AQP4 loss markedly exacerbated neuronal pyroptosis in both the ipsilateral and contralateral cortices Conclusion: Our findings establish AQP4 as a critical suppressor of neuronal pyroptosis after ischemic stroke. It confers protection by enhancing IκBα expression to inhibit NF-κB signaling, thereby dampening NLRP1 inflammasome activation and the subsequent pyroptotic cascade. This study unveils a novel AQP4/IκBα/NF-κB axis in post-ischemic neuroinflammation and highlights AQP4's role in mitigating remote secondary injury, offering new insights for developing neuroprotective strategies targeting global brain resilience.
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