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. 2026 Jul 24;24:471. doi: 10.1186/s12964-026-03023-7

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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 — OTA-induced sEV treatment increased the expression of kidney injury markers in normal kidney cells. A Fluorescent staining confirms the intracellular uptake of NRK52E cell-derived sEVs after 24 h of treatment. B Immunoblotting analysis of the expression of kidney injury markers after 24 h of sEV treatment. C-F Bar diagram representing the densitometry analysis of the expression of clusterin C, B2M D, cystatin C E, and fibronectin F. The data were normalized by the expression of β-actin. C-sEVs = control cells-derived sEV-treated NRK52E cells,LD-sEVs = LD-derived sEV-treated NRK52E cells, and HD-sEVs = HD-derived sEV-treated NRK52E cells