Fig. 1: Mechanism of cell death induced by pyroptosis.
From: Targeting pyroptosis as a preventive and therapeutic approach for stroke
In the classical inflammatory pathway, DAMPs and PAMPs increase the activation of NLRP3 inflammasomes, thereby promoting Caspase-1 cleavage of GSDMD and the pro-inflammatory factors IL-18 and IL-1β, causing pyroptosis; in the non-classical inflammatory pathway, LPS directly induces Caspase-4/5/11 to cleave GSDMD, thereby promoting pyroptosis. In addition to GSDMD, GSDMA/B/C/E can also induce pyroptosis and are not functionally significantly different in that they are cleaved by SpeB (secreted by GAS), Granzyme A, Caspase-8, and Caspase-3, respectively. DAMPs damage-associated molecular pattern molecules; TLR4 toll-like receptor 4, NF-κB nuclear factor kappa-B, NLRP3 NOD-like receptor thermal protein domain associated protein 3, ASC apoptosis-associated speck-like protein containing CARD, IL-18 interleukin-18, IL-1β interleukin-1β, dsDNA double-stranded DNA, LPS lipopolysaccharides, GSDMA/B/C/D/E gasdermin A/B/C/D/E, INF-γ interferon-γ, GAS group A Streptococcus, SpeB streptococcal pyrogenic exotoxin B.
