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. 2020 Feb 25;11:80. doi: 10.3389/fendo.2020.00080

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Copyright © 2020 Shirasuna, Karasawa and Takahashi.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic mechanisms of NLRP3 inflammasome activation. NLRP3 is activated by various endogenous DAMPs: uric acid crystals (MSU), cholesterol crustal, cell-free DNA (cfDNA), high-mobility group box 1 (HMGB1), extracellular debris, extracellular vesicles (EVs), advanced glycation end-products (AGEs), and free fatty acid. Various events such as intracellular ATP release, NLRP3 deubiqutination, relocalization, reactive oxygen species (ROS) generation, mitochondrial dysfunction, lysosome rapture, and cathepsin release occur depending on the effects of damage-associated molecular patterns (DAMPs). Then, inflammasome components, including NLRP3, ASC, and procaspase-1, form the NLRP3 inflammasome complexes. Finally, activated caspase-1 induces the inflammatory form of cell death known as pyroptosis and cleaves the precursor cytokines pro-IL-1β and pro-IL-18, generating the biologically active cytokines IL-1β and IL-18.