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. 2023 Dec 1;14(12):787. doi: 10.1038/s41419-023-06319-5

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© The Author(s) 2023

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. 4 — A Expression of p53-pathway genes involved in pro-apoptosis, anti-apoptosis, intrinsic apoptosis and ferroptosis in Control and HDAC4 and 5 overexpressing C2C12 myoblasts. (Unpaired t-tests). B Apoptotic cells in response to the apoptosis-inducing agent Camptothecin in Control and HDAC4 and 5 overexpressing C2C12 myoblasts. (Two-way ANOVA, genotype p < 0.0001 F(1,12) = 349.3, treatment p < 0.0001 F(2,12) = 270.4, interaction p < 0.0001 F(2,12) = 149.5, significant Tukey’s multiple comparisons shown). C Cell viability in response to the ferroptosis-inducing agent RSL3 in Control and HDAC4 and 5 overexpressing C2C12 myoblasts. (Two-way ANOVA, genotype p < 0.0001 F(1,12) = 1645, treatment p < 0.0001 F(1,12) = 36.09, interaction p < 0.0090 F(1,12) = 9.665, significant Tukey’s multiple comparisons shown). D Cell viability in response to palmitate in Control and HDAC4 and 5 overexpressing C2C12 myoblasts (Two-way ANOVA, genotype p < 0.0001 F(1,12) = 3374, treatment p < 0.0001 F(2,12) = 1012, interaction p < 0.0001 F(2,12) = 684.8, significant Tukey’s multiple comparisons shown). E Apoptotic cells in response to palmitate in Control and HDAC4 and 5 overexpressing C2C12 myoblasts. (Two-way ANOVA, genotype p < 0.0001 F(1,12) = 1468, treatment p = 0.0001 F(2,12) = 20.35, interaction p < 0.0050 F(2,12) = 8.498, significant Tukey’s multiple comparisons shown). F Western blots of full-length (FL) and cleaved (CL) caspase 3 and 9 in response to increasing palmitate concentrations in Control and HDAC4 and 5 overexpressing C2C12 myoblasts. G Lipid peroxidation in response to palmitate (Two-way ANOVA, genotype p < 0.0001 F(1,12) = 313.4, treatment p < 0.0103 F(2,12) = 67.31, significant Tukey’s multiple comparisons shown) in Control and HDAC4 and 5 overexpressing C2C12 myoblasts. Data are mean ± SEM, n = 3–4 biological replicates per group.