Disruption of Ion Homeostasis in the Neurogliovascular Unit Underlies the Pathogenesis of Ischemic Cerebral Edema

摘要: Cerebral edema is a major cause of morbidity and mortality following ischemic stroke, but its underlying molecular pathophysiology incompletely understood. Recent data have revealed the importance ion flux via channels transporters expressed in neurogliovascular unit development ischemia-triggered cytotoxic edema, vasogenic hemorrhagic conversion. Disruption homeostatic mechanisms governing cell volume regulation epithelial/endothelial transport due to ischemia-associated energy failure results thermodynamically driven re-equilibration solutes water across CSF–blood blood–brain barriers that ultimately increases brain’s extravascular volume. Additionally, hypoxia, inflammation, other stress-triggered functional expression normally at low levels disruptions homeostasis contribute cerebral edema. Here, we review pathophysiological significance several mediators unit, including targets existing FDA-approved drugs, which might be potential nodes for therapeutic intervention.