Stent treatment improves cerebral microcirculatory disorder and blood-brain barrier function in internal carotid artery stenosis via intercellular adhesion molecule 1 modulation.

This study investigates the molecular mechanisms of early stent placement intervention in mitigating neurovascular unit damage and cerebral microcirculatory disorder (CMD) associated with severe internal carotid artery stenosis (ICAS). By utilizing a rat model of severe ICAS, early stent placement was found to improve cerebral blood flow, restore blood-brain barrier (BBB) integrity, and alleviate cognitive deficits by downregulating intercellular adhesion molecule 1 (ICAM1) expression. Transcriptomic analysis highlighted ICAM1's role in neurovascular repair by modulating inflammatory pathways and BBB-associated tight junction proteins. In vitro experiments supported that ICAM1 knockdown enhanced BBB function by reducing inflammatory cytokines and promoting cell proliferation and migration. However, rescue experiments demonstrated that ICAM1 overexpression impeded the therapeutic effect of stent placement by exacerbating CMD and BBB disruption through upregulation of matrix metalloproteinase-9 (MMP-9) and inflammatory cytokines. These findings suggest that targeting ICAM1-related pathways could optimize stent treatment strategies, emphasizing the importance of ICAM1 regulation in reducing the risk of watershed infarction and improving therapeutic outcomes in ICAS management.