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. 2017 Oct 13;114(3):401–408. doi: 10.1093/cvr/cvx204

Figure 4.

Figure 4

Endo-Nox4KO exhibit worse load-induced dysfunction than wild-type controls. (A) Nox4 protein expression in aorta of wild-type and endo-Nox4KO mice. *P < 0.05, n = 3, unpaired Student’s t-test. (B) Immunostaining for Nox4. Aortic sections stained for Nox4 (green) and CD31 (red) as an endothelial cell marker. Scale bars 50 μm. The yellow colour in the merged images in the right panels denotes co-localization. (C) Mean data for cardiac hypertrophy in terms of left ventricle weight/body weight ratio (LV/BW) (n = 10/group). (D–H) Echocardiographic analysis of WT and Endo-Nox4KO mice subjected to 6 weeks AAB (n = 10–12/group). IVSD, interventricular septal diameter; LVEDV, LVESV, LV end-diastolic and end-systolic volumes; EF, ejection fraction. **P < 0.01 vs. respective sham controls. #P < 0.05, ##P < 0.01 vs. WT/AAB, two-way ANOVA with Tukey’s Multiple Comparison Test. All data are presented as mean ± SEM.

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