Fig. 7: Schematic drawing of the major finding. | Cell Death & Disease

Fig. 7: Schematic drawing of the major finding.

From: Dexmedetomidine improves the circulatory dysfunction of the glymphatic system induced by sevoflurane through the PI3K/AKT/ΔFosB/AQP4 pathway in young mice

Fig. 7

Sevoflurane inhibits the activation of PI3K/AKT pathway and up-regulates the expression of transcription factor ΔFosB. ΔFosB binds to the AQP4 promoter region, represses AQP4 transcription, and down-regulates its expression. The AQP4 polarity and its expression are down-regulated, resulting in a decrease in the circulation function of the glymphatic system. The accumulation of metabolic waste products in the brain damages neurons and synapses, leading to a long-term decline in learning and memory ability in young mice. Dexmedetomidine alleviates sevoflurane-induced glymphatic dysfunction through PI3K/AKT/ΔFosB/AQP4 pathway.

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