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. 2020 Sep 15;11(9):756. doi: 10.1038/s41419-020-02948-2

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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. 7 — a The mean concentrations of free fatty acids detected by GC-MS in αMHC-Acot1 transgenic mice and their littermates. b Top 5 FFAs concentrations in murine heart tissue. c Cell viability analysis showing different concentrations of FFAs enhanced DIC in HL-1 cells. d Cell viability analysis showing the protective effect of Acot1 overexpression and Fer-1 co-treatment to FFAs enhanced DIC. e Diagrammatic method of showing the opposite enzymatic function of Acsl family and Acot family in the cell. f The potential mechanism of Acot1 inhibits the induction of ferroptosis in DOX-induced cardiotoxicity. LIP liable iron pool, DIC doxorubicin-induced cardiotoxicity, Fer-1 Ferrostatin-1. Significance in b was calculated using the unpaired Student’s t test. Significance in c, d was calculated using the one-way ANOVA test with multiple comparisons between the two groups. P value < 0.05 was considered to be significant, and labeled as *P < 0.05; **P < 0.01; ***P < 0.005; ****P < 0.001; ns not significant.