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Fig. 6 | Fluids and Barriers of the CNS

Fig. 6

From: Pathogenic mechanisms and therapeutic implications of extracellular matrix remodelling in cerebral vasospasm

Fig. 6

Severe vascular stenosis may involve YAP activation and persistent blood stimulation. The potential activation mechanism of YAP involves cell–extracellular matrix (ECM) interactions mediated by the activation of integrins. Enhanced mechanical transmission and reorganisation of the actin cytoskeleton activate YAP/transcriptional co-activator with PDZ-binding motif (TAZ), prompting their nuclear translocation. Activated YAP can mediate various signalling molecules to regulate vascular smooth muscle proliferation, such as the miR-130/301 family, IL-6, endothelin, and fibroblast growth factor. It can also promote ECM deposition by upregulating miRNA-130/301, which in turn activates YAP/TAZ, leading to further remodelling of the ECM and luminal vessel narrowing. Additionally, sustained stimulation of blood vessels may lead to vasoconstriction and severe luminal vessel narrowing

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