Inflammatory signaling pathways and inflammasome components

Inflammatory signaling pathways and inflammasome components constitute a sophisticated network of the innate immune system designed to sense and respond to cellular stress, infection, and tissue damage [1]. At the core of this system are inflammasomes, which are high-molecular-weight multiprotein complexes—most notably the NLRP3 inflammasome—that assemble in the cytosol upon detection of pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs) [1][2]. Activation of these complexes leads to the recruitment and activation of caspase-1, which subsequently processes the pro-inflammatory cytokines interleukin-1β (IL-1β) and interleukin-18 (IL-18) into their active forms and may trigger a form of programmed cell death known as pyroptosis [3][4]. Chronic or aberrant activation of these pathways is a major driver in the pathogenesis of various diseases, including autoinflammatory syndromes, cardiovascular diseases like atherosclerosis, and neurodegenerative conditions such as Alzheimer's disease [5][6]. Pharmacological intervention typically targets these pathways through the use of monoclonal antibodies against IL-1β, IL-1 receptor antagonists, or small-molecule inhibitors of specific inflammasome sensors like NLRP3 [7][8].

Other names

Inflammasome complexIL-1 signaling pathwayPyroptosis pathwayNLRP3 pathway

Inhibition of the NLRP3 inflammasome assembly, neutralization of IL-1β, or competitive inhibition of the IL-1 receptor to prevent downstream inflammatory signaling.