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. 2023 May 11;14(5):318. doi: 10.1038/s41419-023-05830-z

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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 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. 5 — A Identification of differentially expressed genes (DEGs) specifically expressed in AKI-PTCs by the strategy of Supplemental Fig. S14A. The aim was to screen for DEGs specifically expressed in different etiologically induced AKI, which required limiting the expression of Control. B After excluding genes intersected with Control, the number of intersections of PTCs-DEGs for each model. C A total of 18 genes that were specifically highly expressed in PTCs of the AKI dataset were screened. Genes including Havcr1, C3, and Krt20 were identified in the unsupervised setting, which confirmed the reliability of the screening strategy. Kruskal–Wallis test, ****P < 0.0001 vs. PTCs group. D Expression of 18 DEGs in different models of PTCs. E Expression of 18 DEGs in seven different states of PTCs.