Figure 1.

Inflammatory and pathological consequences of pyroptosis (1). Pyroptosis, induced by Gasdermin D (GSDMD) pore formation, results in the release of proinflammatory cytokines, alarmins, and damage-associated molecular patterns (DAMPs). These inflammatory molecules act on bystander cells (e.g., endothelial cells, lymphocytes) to promote an inflammatory response. The resulting cell death and inflammation can disrupt the endothelial barrier in blood vessels and vital organs, such as the lungs, leading to leucocyte infiltration. GSDMD pore formation activates the coagulation cascade and can contribute to lethality from disseminated intravascular coagulation. Pyroptosis in neutrophils and other cells triggers NETosis. Improper neutrophil extracellular trap (NET) and aberrant NETosis and DAMP removal can further induce pyroptosis and tissue damage. Reproduced with permission from [Vasudevan SO, Behl B, Rathinam VA], [Pyroptosis-induced inflammation and tissue damage.]; published by [Semin Immunol], [2023].