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. 2021 Nov 10;7:346. doi: 10.1038/s41420-021-00746-z

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© The Author(s) 2021

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — Based on our findings, we established a model for the mechanisms through which P2X7 affects autophagy and pyroptosis. Briefly, when rats perform high-intensity exercise or chondrocytes receive high-intensity stimulation, P2X7 is overactivated, and the ion flow mediated by P2X7 activates the inflammasome pathway, causing the activation of caspase-1 and the release of active IL-1β. The AMPK/mTOR pathway mediated by P2X7 is insufficient to resist the damage caused by pyroptosis. By contrast, when rats perform moderate-intensity exercise or chondrocytes receive an appropriate intensity of stimulation, P2X7 is moderately activated, and the ion flow mediated by P2X7 mainly activates the AMPK/mTOR pathway, resulting in increased autophagy and enabling the induced autolysosomes to target the degradation of inflammasome components, thereby inhibiting pyroptosis and maintaining chondrocyte activity.