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Mechanistically, the inflammatory human caspase-1/4/5 and mouse caspase-1/11 as well as caspase-3, serine protease, mediate proteolytic cleavage of corresponding gasdermins (GSDMs) and liberate N-terminal (NT) fragments binding to phospholipids in inner plasma membrane to form pores, enabling the release of pro-inflammatory cytokines and plasma membrane rupture 5,6,7,8

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