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. 2021 Jan 21;11:2037. doi: 10.1038/s41598-021-81570-4

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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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SERCA2a regulated calpain activity via [ca²⁺]_i in myocardial I/R mice. (A) The level of SERCA2a protein expression in each group. GAPDH was used as the internal control. The grouping of gels/blots cropped from different parts of the same gel. Uncropped blots are available in Supplementary Fig. 2A. (B) The diastolic [ca²⁺]_i of cardiomyocyte in each group. (C, D) The calpain activity in each group. GAPDH was used as the internal control. The grouping of gels/blots cropped from different parts of the same gel. Uncropped blots are available in Supplementary Fig. 2C. Individual data points are presented in Supplemental Fig. 2A-D. **P < 0.01, ***P < 0.001 versus sham; ^#P < 0.05, ^##P < 0.01, ^###P < 0.001 versus I/R; ^&P < 0.05, ^&&&P < 0.001 versus PD + I/R; ^$$$P < 0.001 versus SERCA2a KO; ^{^^^}P < 0.001 versus SERCA2a KO + I/R; ^@@P < 0.01, ^@@@P < 0.001 versus Ad-GFP + I/R. n = 3; mean ± SEM.