ArticleFrontiers in aging neuroscience2026
Astragaloside IV attenuates hypoxia-reoxygenation-induced endothelial senescence and vascular inflammation by modulating the NOTCH1/VCAM-1 axis.
Article in Frontiers in aging neuroscience, 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
Objective: Alzheimer's disease (AD) progression involves cerebral microvascular endothelial cell senescence induced by brain hypoperfusion, which contributes to blood-brain barrier (BBB) dysfunction. While Notch1 signaling is known to exacerbate endothelial senescence and neuroinflammation via vascular cell adhesion molecule-1 (VCAM-1), the mechanism by which it mediates hypoxia-induced endothelial aging in AD remains unclear. Furthermore, although Astragaloside IV (AS-IV) has been shown to alleviate cerebral hypoperfusion in AD, whether it acts by directly modulating the Notch1/VCAM-1 axis is unknown. This study aimed to determine whether AS-IV mitigates endothelial senescence and AD pathology by modulating the Notch1/VCAM-1 pathway. Methods: Transcriptomic analysis of AD patient data and network pharmacology identified Results: Conclusion: AS-IV alleviates HR-induced endothelial senescence by modulating the Notch1/VCAM-1 axis. Our data suggest that AS-IV does not merely inhibit Notch1 but acts by modulating its signaling toward a protective equilibrium, thereby attenuating endothelial senescence and inflammation associated with the restoration of Notch1/VCAM-1 signaling balance. These findings highlight the potential of AS-IV as a therapeutic candidate for AD vascular pathology.
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