Neutrophil RAGE drives early cerebrovascular injury after subarachnoid hemorrhage
An international research team from Japan and the United States, led by Assistant Professor Hiroshi Ishii and Professor Osamu Hori, together with Professors Yasuhiko Yamamoto and Mitsutoshi Nakada of Kanazawa University, has identified neutrophil RAGE (receptor for advanced glycation end products) as a key driver of early cerebrovascular injury after subarachnoid hemorrhage (SAH).
An international research team led by Assistant Professor Hiroshi Ishii and Professor Osamu Hori has identified neutrophil RAGE (receptor for advanced glycation end products) as a key driver of early cerebrovascular injury after subarachnoid hemorrhage (SAH). The study, published in the Journal of Cerebral Blood Flow & Metabolism, shows that neutrophil RAGE promotes neutrophil accumulation around cerebral arteries, cerebral vasospasm, impaired cortical circulation and neurological dysfunction.
The findings suggest that an immediate sympathetic vascular response is followed by a neutrophil RAGE-dependent inflammatory phase, which may help identify earlier, mechanism-based therapeutic strategies for SAH.
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