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. 2023 Jul 17;14(7):442. doi: 10.1038/s41419-023-05947-1

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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. 7 — In early DKD, lower percentages of proliferative PT and PT^AQP4+ induced impaired cell repair activity and dysfunction of RAS modulation. CP acted as a central regulator of the induction of ferroptosis in PT^AQP4+. Lower percentages of TAL and CD with impaired metabolism function were pathogenic features. SPP1 mediated pathogenic cross-talk in the tubular microenvironment. MC-derived SEMA3C further promoted endothelium-mesenchymal transition in GEC through NRP1 and NRP2 pathway.