ArticleNeuroscience bulletin2026
Endothelial GATAD1 Exacerbates Blood-brain Barrier Dysfunction in Ischemic Stroke through Caveolae-mediated Transcytosis.
Article in Neuroscience bulletin, 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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Abstract
Blood-brain barrier (BBB) dysfunction represents a critical pathological manifestation in exacerbating ischemic stroke, contributing to neuronal death, edema formation, and unfavorable clinical outcomes. GATA zinc finger domain-containing 1 (GATAD1) is recognized as a critical transcription factor in cardiac development and cardiovascular disease. However, the role of GATAD1 in regulating BBB function and ischemic stroke remains elusive. Here, we found that GATAD1 was upregulated in cerebral endothelial cells (ECs) following ischemic stroke in mice. EC-specific Gatad1 deficiency demonstrated remarkable neuroprotection, manifested by reduced infarct volumes, ameliorated BBB dysfunction, and improved neurological outcomes following experimental stroke. Mechanistic investigations revealed that GATAD1 was involved in regulating CD36 expression, thereby modulating caveolae-mediated transcytosis in cerebral ECs. These findings established GATAD1 as a novel regulator of BBB permeability and a potential therapeutic target for ischemic stroke intervention.
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