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. 2024 Jun 22;4(3):298–312. doi: 10.1007/s43657-023-00140-y

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© The Author(s) 2024

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/.

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Fig. 5 — Schematic and validation of sonodynamic therapy (SDT)-induced pyroptosis. a The design of SDT-pyroptosis nanoparticle; b Validation of morphological changes and effectors of SDT-induced pyroptosis. The sonodynamic nanoparticles were responsive to the low-pH microenvironment of tumors. Chlorin e6 (Ce6) could exert the sonodynamic effect on tumor cells upon irradiation of low-frequency ultrasonic beams by producing cytotoxic reactive oxygen species (ROS). The SDT process consumed oxygen and attenuated hypoxia in cells, enhancing the cell-killing effect of tirapazamine (TPZ). SDT and chemotherapy of TPZ could synergistically trigger pyroptosis of tumor cells. And SDT induced pyroptosis through the caspase-1/GSDMD pathway. The involvement of pyroptosis was verified by detecting cell pyroptotic changes and producing pyroptotic products (Yu et al. 2022). The figure was created with BioRender.com. Printed with permission from Frontiers in Bioengineering and Biotechnology. Copyright 2022, Yu, Cao, Han, Wang, Qiu, Wang, Wei, Wang, Zhang, Liu, Mo and Chen