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. 2022 Jul 8;12:11684. doi: 10.1038/s41598-022-15743-0

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© The Author(s) 2022

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 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/.

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HDAC1-induced PFKM transcriptional repression regulated DOX-mediated OXPHOS and glycolysis in H9c2 cells. H9c2 cells were transfected with PFKM siRNA or nonspecific siRNA (siNC) and treated with 2 μM DOX in the absence or presence of 0.1 μM MGCD for 24 h, and (A) cell viability, (B) OCR and (C) ECAR, (D) ATP and (E) lactate level were measured. (F) Schematic representation of the regulation of DOX-induced cardiotoxicity via OXPHOS and glycolysis through HDAC1-induced PFKM transcriptional repression. ***P < 0.001 vs Control; ^###P < 0.001 vs DOX + siNC + vehicle; ^ΔΔP < 0.01 vs DOX + siPFKM-1 + vehicle.