Authors
Ruilin Chen, Xun Zhang, Enjie Song, Xin Chen, Ming Wang, Shanhu Xu, Fengli Fu, Jian He, Shu Wan
Published in
Reviews in the neurosciences. Oct 22, 2026. Epub Oct 22, 2026.
Abstract
Stroke triggers a complex secondary injury cascade, in which neuroinflammation plays a central role. The glymphatic system is a perivascular clearance network that facilitates cerebrospinal fluid (CSF) and interstitial fluid (ISF) exchange and removes metabolic waste from the brain. Recent studies suggest that glymphatic dysfunction is not simply a consequence of stroke, but also contributes to disease progression. Impaired glymphatic clearance promotes the accumulation of damage-associated molecular patterns, inflammatory mediators, and toxic metabolites within the brain parenchyma, sustaining both innate and adaptive immune responses. At the same time, inflammatory signaling, immune cell infiltration, and vascular injury progressively disrupt perivascular architecture and aquaporin-4 (AQP4) polarization, leading to further impairment of glymphatic transport. As a result, glymphatic dysfunction and neuroinflammation reinforce each other, contributing to cerebral edema, persistent inflammation, and neurological deterioration after stroke. In this review, we summarize current evidence linking glymphatic dysfunction to neuroinflammation in both ischemic and hemorrhagic stroke. We discuss the molecular and cellular mechanisms underlying this interaction and preclinical therapeutic approaches that may help preserve or restore glymphatic function after stroke. A better understanding of the relationship between glymphatic dysfunction and neuroinflammation may reveal new therapeutic opportunities for improving neurological recovery after stroke.
PMID:
42904435
Bibliographic data and abstract were imported from PubMed on 23 Oct 2026.
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