Our study identifies the S1PR1-CCN1 axis as a critical regulator of endothelial plasticity in bAVMs. S1PR1 knockdown promotes an EndoMT-like phenotype and enhances endothelial migration, although CCN1 acts as a downstream effector mediating these changes. The in vivo findings in zebrafish further highlight the role of this axis in cerebrovascular instability. Targeting this pathway may offer new therapeutic opportunities to mitigate bAVM progression and rupture risk.
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Li et al. (2025) studied this question.
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