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

Figure 1.

Figure 1

Nox4-null mice have exaggerated cardiac hypertrophy and dysfunction in response to TAC. (A) Left ventricle/body weight (LV/BW) ratio 2 weeks after TAC (n = 10–14/group). (BD) Echocardiographic analysis of WT and Nox4KO mice subjected to 2 weeks TAC (n = 10/group). IVSD, interventricular septal diameter; EF, ejection fraction. (EF) Mean data for myocardial interstitial fibrosis and capillary density (n = 7–9/group). (GI) Protein levels of VEGF-A, HIF1α, p-eNOS, and total eNOS in LV of Nox4-null mice compared to WT. Representative immunoblots are shown at the top and mean data below (n = 4/group). VEGF, vascular endothelial growth factor; HIF1α, hypoxia-induced factor-1α; eNOS, endothelial nitric oxide synthase. *P < 0.05, **P < 0.01 vs. respective sham controls. #P < 0.05, ##P < 0.01 vs. WT/TAC, two-way ANOVA with Tukey’s Multiple Comparison Test. All data are presented as mean ± SEM.

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