虚血性脳卒中後の免疫介在性血液脳関門破壊：メカニズムと治療標的

Ischemic stroke is an acute cerebrovascular disorder characterized by the obstruction of cerebral arteries, leading to focal cerebral ischemia and infarction, ultimately resulting in neurological deficits. Its pathogenesis involves a cascade of immune-inflammatory responses and blood-brain barrier (BBB) disruption. Emerging evidence highlights that immune inflammation is a central driver of post-stroke brain injury. Microglial activation, neutrophil infiltration, and the release of pro-inflammatory cytokines collectively exacerbate BBB breakdown and neuronal death. Concurrently, these immune processes participate in tissue remodeling and repair. Notably, the interplay between immune-mediated inflammation and BBB damage forms a vicious cycle that aggravates neurological outcomes and hampers recovery. This review focuses on the molecular mechanisms of ischemia and hypoxia-induced BBB dysfunction, and the immunological processes involved, aiming to provide insights into multi-target and temporally precise neuroprotective strategies for ischemic stroke.