Fig. 10.

Schematic diagram for the mechanisms of LDLR in the regulation of neuronal pyroptosis following cerebral ischemia. The expression of LDLR is downregulated after Cerebral I/R. LDLR restrains two-step processing pathways, including NF-κB signaling (priming) and NLRP3-ASC-caspase-1 inflammasome assembly, to mitigate generating inflammatory mediators and cytokines. The triggered caspase-1 cleaves GSDMD to promote the release of N-terminal domain, which executes pores formation on neuronal membrane. The mature forms of IL-18 and IL-1β secreted through these pores are also alleviated, which facilitates anti-inflammatory effect post-stroke