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. 2021 Sep 8;11:17808. doi: 10.1038/s41598-021-97449-3

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© The Author(s) 2021

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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MCU KO hearts are protected from CaMKII activation caused by HFD and have fewer sparks and fewer spontaneous contractions. (A) Immunoblots of phospho-CaMKII, oxy-CaMKII, and total CaMKII from heart lysates. (B) Graph of immunoblots phospho-CaMKII corrected for total CaMKII. (C) Representative images of calcium sparks. (D) Graph of quantification of calcium sparks, n = 12–20 cardiomyocytes from 3 isolations, *indicates significantly different by post-hoc test. KN93 is a CamKII inhibitor, 0.5 µM. (E) Graph of quantification of spontaneous beats following pacing in cardiomyocytes. (F) Representative images of single cell contractility and spontaneous beats following pacing. (G) Representative images of oxidized RyR2, measured by DNP modification, phosphorylated RyR2 (ser2814) and total RyR2. (H) Graphs of quantification of oxidized RyR2 and P-RyR2 (normalized to total RyR2), both are sig different by ANOVA, *Indicates significantly different from control chow by post-hoc test.