Pyroptosis is a programmed cell death process executed by inflammatory caspases upon initiation of canonical or non-canonical mechanisms. It is triggered by specific inflammatory caspases (caspase-1, -4, -5, -11) that are distinct from those responsible for apoptosis. Both the canonical and non-canonical pathways lead to the activation of gasdermin D (GSDMD), which forms pores that cause cellular leakage and lysis. The canonical sequence involves pathogen-associated molecular patterns (PAMPs)- and damage-associated molecular patterns (DAMPs)-mediated inflammasome formation leading to caspase-1 activation, GSDMD cleavage, and IL-1β and IL-18 maturation. The non-canonical string of events is characterized by direct interaction of the other three caspases with Gram-negative bacterial lipopolysaccharide (LPS) with subsequent GSDMD activation. The resultant extracellular release of cytoplasmic components unleashes a local inflammatory cascade that can become systemic, underscoring the importance of pyroptosis’ normal function in mobilizing immune cells against pathogens. Nevertheless, pyroptosis can also contribute to inflammation-related pathology, including cancer progression and autoimmune disease.

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