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. 2021 Jan 19;13:7. doi: 10.1186/s13098-021-00625-8

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© The Author(s) 2021

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. 5 — OXSR1 was a direct target of miR-93-5p. a The potential binding sites between miR-93-5p and OXSR1 were exhibited. b, c Dual-luciferase reporter assay and RIP assay were performed to verify whether OXSR1 could interact with miR-93-5p. d The mRNA level of OXSR1 in the serums of septic AKI patients (n = 19) and healthy controls (n = 19) was measured by qRT-PCR assay. e The correlation between OXSR1 mRNA and miR-93-5p in the serums of septic AKI patients was analyzed by Spearman’s correlation coefficient analysis. f The protein expression of OXSR1 in HK2 cells treated with different concentrations of LPS was quantified by western blot. g The protein level of OXSR1 in LPS-induced HK2 cells with miR-93-5p knockdown or overexpression was tested by western blot. **P < 0.01, ***P < 0.001, ****P < 0.0001