Fig. 8
From: Role of SPAK–NKCC1 signaling cascade in the choroid plexus blood–CSF barrier damage after stroke
Schematic summary of stroke-induced dysregulation of the blood–CSF barrier via SPAK–NKCC1 signaling pathway. Ischemic stroke activation of SPAK–NKCC1 cascade in the ChP. Overstimulation of SPAK–NKCC1 signaling pathway activity leads to TJ damage, blood–CSF barrier dysfunction, and immune cell infiltration at the ChP. Ischemic reperfusion-mediated production of ROS can directedly activate SPAK–NKCC1 cascade and MMP9 protein expression with NF-κB activation as an upstream mechanism. Pharmacological inhibition of the SPAK–NKCC1 cascade attenuates blood–CSF barrier damage and brain inflammation