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. 2026 Jan 19;16:2415. doi: 10.1038/s41598-025-23316-0

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© The Author(s) 2026

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, 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 you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. 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-nc-nd/4.0/.

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Fig. 3 — Representative morphological, SWE imaging and molecular changes in tubules after administration of anti-Fx1A, L-NAME or their combination. Compared with vehicle treated animals, L-NAME administration alone or with anti-Fx1A for 7 weeks caused fibrosis in the interstitium as revealed in H&E (A) and PSR (B) stained renal sections. (C) AI-enabled image analysis revealed increased total PSR-stained areas (p < 0.05) in the combination group compared with vehicle control group. In vivo renal stiffness was significantly (p < 0.05) higher in all three treatment groups on day 44 but not on day 23 (D). ELISA revolve that fibroblastic marker αSMA increased significantly (p < 0.05) on day 49 in the combination group animals compared with the vehicle group (E).