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Inflammasome activation refers to the assembly and activation of multiprotein inflammasome complexes in response to cellular damage or infectious signals. Key inflammasome types (NLRP3, AIM2, NLRC4, NLRP1, and PYRIN) serve as intracellular sensors for pathogen- and damage-associated molecular patterns, leading to the recruitment of the adaptor protein ASC and pro-caspase-1. This results in the activation of caspase-1, which cleaves pro-inflammatory cytokines IL-1β and IL-18 into their mature forms and induces pyroptotic cell death via gasdermin D pore formation. Dysregulated inflammasome activation plays a central role in the pathogenesis of various inflammatory, metabolic, neurodegenerative, and cardiovascular diseases. Multiple drugs in clinical development target individual inflammasome proteins, particularly NLRP3, rather than the activation process as a whole[2][4][1][3][5][6].
Inhibition of NLRP3 assembly (e.g., small molecule NLRP3 inhibitors); Blocking caspase-1 activation; Preventing ASC oligomerization; Inhibiting IL-1β/IL-18 maturation and secretion
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