ReviewCells2025
Glymphatic Dysfunction in Neuro-Pulmonary Complications Following Subarachnoid Hemorrhage: A New Perspective on Brain-Lung Axis Disruption.
Review in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Review
- Brain Lymphatic Dysfunction in Subarachnoid Hemorrhage: Pathophysiology and Clinical Implications.Biomolecules · 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
2 authors.
Funding
Abstract
Subarachnoid hemorrhage (SAH), often resulting from aneurysmal rupture, remains a life-threatening cerebrovascular disorder with high morbidity and mortality. While previous research has focused primarily on cerebral damage and neurological outcomes, growing evidence suggests that SAH also causes systemic complications, including pulmonary dysfunction. The underlying mechanisms linking SAH to lung injury, however, are not fully understood. The glymphatic system, a perivascular network that facilitates the clearance of cerebrospinal fluid (CSF) and interstitial waste from the brain, plays a critical role in maintaining central nervous system (CNS) homeostasis. Aquaporin-4 (AQP4) water channels, predominantly expressed in astrocytic end feet, are essential for efficient glymphatic flow. Emerging studies have shown that SAH impairs glymphatic function by disrupting AQP4 polarity and CSF circulation, resulting in the accumulation of neurotoxic substances and neuroinflammation. Recent findings further suggest that glymphatic dysfunction may exert systemic effects beyond the CNS, contributing to a breakdown of the brain-lung axis. The release of pro-inflammatory cytokines, blood degradation products, and damage-associated molecular patterns (DAMPs) into systemic circulation can promote pulmonary endothelial injury and trigger immune responses in the lungs. This phenomenon is exacerbated by impaired clearance via the glymphatic system, amplifying systemic inflammation and increasing the risk of acute lung injury (ALI) or neurogenic pulmonary edema (NPE). This review proposes a novel perspective linking glymphatic impairment with pulmonary complications after SAH. Understanding this connection could open new therapeutic avenues-such as targeting AQP4 function, enhancing CSF circulation, or modulating the inflammatory response-to mitigate both neurological and respiratory sequelae in SAH patients.
Indexed as
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What Socratic holds
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 Socratic graph.