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. 2023 Jul 28;21:185. doi: 10.1186/s12964-023-01177-2

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — The activation of NLRP3 inflammasome. The priming signal (signal 1) is provided by microbial components or endogenous cytokines, leading to the activation of the transcription factor NF-κB and subsequent upregulation of NLRP3 and pro-IL-1β. The activating signal (signal 2) is from RNA virus, pore-forming toxins, or particulate matter activates the NLRP3 inflammasome with the help of ROS as a by-product of oxidative phosphorylation from mitochondria. (RNA: Ribonucleic acid; TLR: Toll-like receptor; Sirt1: Silent information regulator 2 homolog 1; ROS: Reactive oxygen species; NLRP3: NACHT, LRR and PYD domains-containing protein 3; ASC: a protein; IL: Interleukin; NF-κB: Nuclear factor kappa B)