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. 2021 Jan 13;295(49):16840–16851. doi: 10.1074/jbc.RA119.011890

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© 2020 © 2020 Liang et al.

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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Deletion of Capns1 inhibits tail suspension-induced oxidative stress in mouse hearts. Mice with cardiomyocyte-specific deletion of Capns1 (KO) and their WT littermates (WT) were subjected to TS for 28 days. Oxidative stress was assessed by measuring ROS production (A), MDA production (B), and protein carbonyl content (C) in mouse hearts. Data are mean ± S.D. (error bars), n = 4–7 in each group. Two-way ANOVA followed by Newman–Keuls test was performed for statistical analysis. A, interaction, F = 3.358, p = 0.0855; row factor, F = 5.995, p = 0.0263; column factor, F = 5.915, p = 0.0271. B, interaction, F = 9.633, p = 0.0073; row factor, F = 1.004, p = 0.3322; column factor, F = 12.56, p = 0.0029. C, interaction, F = 7.275, p = 0.0194; row factor, F = 2.682, p = 0.1274; column factor, F = 9.306, p = 0.0101. *, p < 0.05 versus sham + WT; †, p < 0.05 versus TS + WT.