ArticleScientific reports2025
The ADMA-NO-NOX2 axis and its association with leptomeningeal collateral impairment in acute ischemic stroke.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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1 citing paper in PubMed.
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13 authors.
Funding
Abstract
Leptomeningeal collateral (LMC) circulation helps preserve brain tissue during acute ischemic stroke (AIS), with poor collateral status predicting worse outcomes. This study assessed the association between asymmetric dimethylarginine (ADMA), LMCs, infarct volume, and oxidative stress in 101 AIS patients with large vessel occlusion within 6 h or wake-up stroke. LMC status was graded using the Menon score (poor, intermediate, or good) on CT angiography, and recanalization was assessed by the modified Thrombolysis in Cerebral Infarction score. Serum ADMA, NADPH oxidase 2 (NOX2), and nitric oxide (NO) levels were measured at admission (< 6 h, T0), 24 h (T1), and 48 h (T2). Among patients, 43.1% had good, 35.3% intermediate, 21.6% poor LMC status. Higher admission ADMA levels were significantly associated with poor LMC at T0 (p = 0.028) and more severe neurological deficits at T1 and T2 (p = 0.005, p = 0.008). ADMA levels increased over time (p = 0.046), and correlated with NOX2 at T1 (p < 0.001). Rising NOX2 was associated with increased neutrophils (p = 0.013) and decreased lymphocytes (p = 0.006). ADMA may impair endothelial function by reducing NO availability and enhancing NOX2-driven oxidative stress. These findings support a role for the ADMA-NO-NOX2 axis in limiting collateral circulation. Targeting this axis may represent a therapeutic strategy to improve outcomes in AIS.
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