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. 2022 Jan 18;9:789948. doi: 10.3389/fcell.2021.789948

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Copyright © 2022 Yang, Hu, Bian, Yao, Wang, Liu, Guo, Zhang and Peng.

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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The relationship between pyroptosis and osteoarthritis (OA). Pyroptosis: DAMPs and TLRs can interact to exacerbate the inflammatory response. TLRs initiate a signaling cascade leading to cell activation, increased release of the NLRP3 inflammasome, activation of NF-κB and MAPK signaling pathway, and production of associated inflammatory factors (including TNF, IL-12, IL-6, IL-8 and pro-IL-1β) that in turn activate a strong inflammatory response. The inflammatory response promotes the increased release of IL-1β and IL-18 on the cartilage surface exacerbating cartilage damage and also enhancing pyroptosis signaling. The NLRP3 inflammasome can activate caspase-1 which further activates GSDMD to undergo shearing to form the N-terminal end. The N-terminal end of GSDMD leads to cell membrane perforation and ultimately induces pyroptosis. Caspases-4/5/11 are also able to activate GSDMD and can induce pyroptosis.