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. 2020 Oct 28;11(10):929. doi: 10.1038/s41419-020-03135-z

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© The Author(s) 2020

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. 1 — HK-2 cells were treated with 1 μM ferrostatin-1 (Fer-1), 10 μM erastin or not 1 h before the H/R induction. A Fer-1 inhibited the decrease of cell viability induced by H/R. Fer-1 inhibited the increase of iron level induced by H/R. C Fer-1 inhibited the increase of Lipid ROS level induced by H/R. D Fer-1 inhibited the increase of mitochondrial superoxide level induced by H/R. E Fer-1 inhibited H/R-induced cell death. F Heat map showing expression profiles for the H/R-induced and G erastin-treated cells compared with the control group. H Venn diagram showed the intersection of the aberrantly expressed miRNAs in H/R-induced and erastin-treated cells. I, J Upregulation of miR-182-5p and miR-378a-3p in the H/R-induced and erastin-treated HK-2 and TCMK-1 cells were verified by qRT-PCR. n = 6. Data are presented as the mean ± s.e.m. of three independent experiments. **P < 0.01, ***P < 0.001 vs. indicated group.