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. 2022 Jul 15;13:297. doi: 10.1186/s13287-022-02986-x

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. 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/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — A sequential work flow to illustrate the experimental design. First, we isolated and identified USCs and USC-Exo. To investigate the effect of USC-Exo on the IRI-induced kidney injury and ferroptosis, IRI-AKI mice were treated with USC-Exo or ferroptosis inhibitor Fer-1 or vehicle before IRI 15 min. Next, we explored the functional mechanism in vitro. Whether lncRNA TUG1 carried by USC-Exo affected H/R-induced ferroptosis in HK-2 cells was then determined. In addition, whether lncRNA TUG1 regulated ACSL4 mRNA stability by interacting with SRSF1 was proved. Further, we measured the inhibitory effects of lncRNA TUG1 on ferroptosis through SRSF1/ACSL4 axis in HK-2 cells. Finally, the in vivo impact of lncRNA TUG1 on ferroptosis and kidney injury was assessed via overexpressing TUG1 and ACSL4 in mice