Fig. 8.

Schematic diagram for the mechanisms of ChemR23 signaling in neuronal pyroptosis following cerebral ischemia. ChemR23 knockout or inhibition triggers NLRP3-ASC-caspase-1 inflammasome activation, leading to increased inflammatory cytokines IL-18 and IL-1β. The triggered caspase-1 cleaves GSDMD to promote the release of N-terminal domain, which further executes pore formation on the neuronal membrane. On the other hand, ChemR23 agonists (RvE1 or C-9) or overexpression of ChemR23 can reverse the above molecular pathway abnormalities