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. 2023 Jul 13;33(9):679–698. doi: 10.1038/s41422-023-00844-w

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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–h H9c2 cells (a) or myocardial tissues (b) were lysed and immunoprecipitated using anti-SIRT1 antibody or control IgG, followed by detection of α-MHC. H9c2 cells (c) and myocardial tissues (e) treated with or without SIRT1 activator were lysed and immunoprecipitated using anti-α-MHC antibody or control IgG, followed by detection of α-MHC K1897 Lactyl Lysine. H9c2 cells (d) and myocardial tissues (f) treated with or without SIRT1 inhibitor were lysed and immunoprecipitated using anti-α-MHC or control IgG, followed by detection of α-MHC K1897 Lactyl Lysine. H9c2 cells (g) and myocardial tissue (h) treated with or without Ang II were lysed and immunoprecipitated using anti-SIRT1 antibody or control IgG, followed by detection of α-MHC. i Schematic of experimental intervention patterns (control, Ang II, SIRT1 activator, combination of Ang II and SIRT1 activator) in mice and H9c2 cells. j, k H9c2 cells (j) and myocardial tissues (k) indicated in i were lysed and immunoprecipitated using anti-Titin or control IgG, followed by detection of α-MHC. l Quantification of the interaction of α-MHC with Titin and the relative expression level of α-MHC K1897 Lactyl Lysine in k. Tubulin was used as an internal reference (n = 3 per group). m Schematic of experimental intervention patterns (control, Ang II, SIRT1 inhibitor, combination of Ang II and SIRT1 inhibitor) in mice and H9c2 cells. n, o H9c2 cells (n) and myocardial tissues (o) indicated in m were lysed and immunoprecipitated using anti-Titin or control IgG, followed by detection of α-MHC. p Quantification of the interaction of α-MHC with Titin and the relative expression level of α-MHC K1897 Lactyl Lysine in o. Tubulin was used as an internal reference (n = 3 per group). Data are presented as mean ± SD (l, p). Statistical significance was assessed by two-way ANOVA with Bonferroni multiple comparisons test (P values adjusted for 6 comparisons; ns, no significance; *P < 0.05; **P < 0.01; ***P < 0.001).