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. 2019 Jul 31;29(9):754–766. doi: 10.1038/s41422-019-0208-x

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© The Author(s) 2019

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. 5 — NDUFAB1 overexpression protects the heart against IR injury. TG and WT male littermates of 2–4 months old were used. a Alleviated myocardial ROS production in TG hearts. Confocal images of DCF-stained myocardium after Langendorff perfusion and IR injury. Ischemia (IS) was mimicked by stopping perfusion. See Supplementary information, Fig. S19a for experimental protocol. Scale bars, 20 μm. b Statistical analysis of a (mean ± s.e.m.; n = 32–51 image frames from 4–7 male mice per group; **p < 0.01 versus WT, ^#p < 0.01 after IR versus basal). c Rotenone (Rot)-sensitive H₂O₂ production at complex I in WT and TG cardiac mitochondria (mean ± s.e.m.; n = 6 male mice per group; **p < 0.01 versus WT). Succinate (Succ, 5 mM) was used as the substrate of complex II and H₂O₂ was measured with Amplex red. d Images for simultaneous measurement of ∆Ψ_m (TMRM, pseudocolor: red) and cardiomyocyte death (EBD uptake, pseudocolor: green) in Langendorff-perfused hearts subjected to IR injury. Note that all cells with intact ∆Ψ_m are EBD-negative, and all EBD-positive cells display loss of ∆Ψ_m, but not vice versa. Scale bars, 50 μm. e, f Percentages of cells with loss of ∆Ψ_m (e) and EBD-positive cells (f) (mean ± s.e.m.; n = 9–10 male mice per group; *p < 0.05 versus WT, ^#p < 0.01 after IR versus basal). g Representative cross-sections of WT and TG hearts after IR injury. See Supplementary information, Fig. S19b for the experimental protocol. White, infarcted area (IF); red, rest of the area at risk (AAR); blue, tissue not at risk. The AAR was demarcated by dotted line. Scale bar, 1 mm. h, i Statistical analysis of AAR (h) and IF (i) reported as the ratios of AAR to left ventricular area (LV) and IF to AAR (n = 5–8 male mice per group; **p < 0.01 versus WT). j Measurement of serum LDH release after IR (n = 10–13 male mice per group; *p < 0.05 versus WT, ^#p < 0.01 after IR versus basal). k Echocardiographic analysis of cardiac function 48 h after IR injury. EF, ejection fraction; FS, fractional shortening (mean ± s.e.m.; n = 4 male mice per group; *p < 0.05 versus WT)