Key result
NOX5 overexpression disrupts endothelial junctions and increases cerebral immune infiltration during ischemic stroke.
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NOX5 promotes dysregulation of endothelial junctions and cytoskeletal changes, leading to increased immune cell infiltration in the brain during proinflammatory states like ischemic stroke.
we analyzed the potential effects of NOX5 on the infiltration of immune cells to the brain. NOX5 overexpression dysregulated EJs and increased permeability in hCMEC/D3 cells. In HUVECs, overexpression of NOX5 promoted the remodeling of the cytoskeleton and increased inflammatory cell adhesion and infiltration. Under inflammatory conditions, such as those present in ischemic stroke, mice expressing endothelial NOX5 exhibited an increase in the infiltration of immune cells in the brain across the vasculature of the non-infarcted (contralateral) hemisphere and increased inflammatory markers in the infarcted (ipsilateral) hemisphere. NOX5 promotes the dysregulation of EJs and cytoskeletal changes in endothelial cells, which leads to an increased immune cell infiltration in the brain at proinflammatory situations.
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Marqués et al. (2026) studied Ischemic stroke. NOX5 overexpression was evaluated on Immune cell infiltration and endothelial junction permeability. NOX5 overexpression promoted dysregulation of endothelial junctions and increased immune cell infiltration in the brain under inflammatory conditions such as ischemic stroke.
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