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Potential mechanistic pathway by which 17-AAG regulates inflammation and neurogenesis after SAH. SAH damage causes HSP90 upregulation, which leads to P2X7R activation and stimulates NLRP3 inflammasome assembly. The resultant maturation of IL-1β is responsible for the inflammation and reparative neurogenesis. 17-AAG inhibits HSP90, resulting in attenuated inflammation and increased neurogenesis.
