ArticleStroke2026
Leptomeningeal Collaterals Constitute an Immune-Responsive Vascular Niche in Ischemic Stroke.
Article in Stroke, 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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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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7 authors.
Funding
Abstract
backgroundLeptomeningeal collaterals form a critical vascular network that enlarges to support retrograde reperfusion after ischemic stroke, yet the cellular mechanisms governing their structural plasticity remain poorly defined. Here we identify an immune-responsive vascular niche and uncover a central role for bone marrow-derived monocytes in regulating collateral remodeling.
methodsGFP (green fluorescent protein)
resultsWe observed rapid recruitment of EphA4-expressing monocytes to pial collateral vessels after permanent middle cerebral artery occlusion. EphA4 knockout chimeric mice show a marked increase in monocyte recruitment, enhanced collateral diameters, improved cerebral blood flow, reduced infarct volume, and accelerated motor recovery. EphA4-null macrophages exhibited elevated Tie2, p-Akt, and PI3Kα, a phenotype reversed by PI3Kα inhibition or sTie2. We further show enhanced permanent middle cerebral artery occlusion-induced collateral enlargement, neuroprotection, and monocyte recruitment using
conclusionsTogether, these findings establish immune cell-intrinsic EphA4/Tie2 signaling as a key regulator of leptomeningeal collateral enlargement and reveal a therapeutic axis for augmenting perfusion after stroke.
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