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. 2022 Feb 28;8:90. doi: 10.1038/s41420-022-00894-w

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© The Author(s) 2022

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 — a–e Representative confocal microscopy images of sections from kidneys harvested in NC, CS, CS + DMF and DMF group mice stained for iNOS, Arg1, RIG-I, cleaved-Caspase1, N-GSDMD, and cleaved-IL-1β (green), F4/80 (red) and DAPI (blue) (scale bar: 100 μm). n = 6. f The model of myoglobin induced macrophage polarization and pyroptosis in CS-AKI. Mice decompressed after 16 h continuous compression with a 1.5 kg weight have damage to the muscles of their legs, and the necrotic muscles release myoglobin, which reaches the kidneys with the blood circulation and leads to the polarization of the kidney macrophages toward M1 type and pyroptosis. Raw264.7 macrophages treated with ferrous myoglobin to mimic cell model of CS-AKI in vitro promote macrophage polarization and pyroptosis via RIG-I/Caspase1/GSDMD signaling pathway. And promotes mature IL-18 and IL-1β release. Pyroptosis inhibitor DMF can inhibit macrophage polarization and pyroptosis in CS-AKI.