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. 2018 Jun 26;7(13):e008654. doi: 10.1161/JAHA.118.008654

Figure 3.

Figure 3

Cardiac‐specific carboxyl‐terminal modulator protein (CTMP) overexpression ameliorates pathological cardiac hypertrophy induced by pressure overload. A, The ratios of heart weight (HW)/body weight (BW), lung weight (LW)/BW, and HW/tibia length (TL) in nontransgenic (NTG) and transgenic (TG) mice 4 weeks (4W) after sham or aortic banding (AB) surgery (n=11–13 mice per group). B, Representative images of hematoxylin and eosin–stained hearts from each group (n=6–7 mice per group; bar=50 μm), and statistical results for the cardiomyocyte cross‐sectional area (n>100 cells per group). C, Quantitative analysis of left ventricular (LV) end‐diastolic diameter (LVEDd), LV end‐systolic diameter (LVESd), and fractional shortening (FS) in each group 4W after AB surgery (n=10–13 mice per group). D, Representative images of picrosirius red–stained hearts from each group (n=6–7 mice per group; bar=100 μm), and statistical results for fibrotic areas in each group (n>30 fields per group). E and F, Real‐time polymerase chain reaction analyses of the hypertrophic (E) and fibrotic (F) markers in each group (n=4 per group). **P<0.01 vs NTG sham; ## P<0.01 vs NTG AB (A through F) by Tamhane's T2 analysis (A [HW/BW], B, C [LVESd], D, E [Bnp and Myh7], and F [Collagen III]) or Bonferroni post hoc analysis (A [LW/BW and HW/TL], C [LVEDd and FS], E [Anp], and F [Collagen Iα and Ctgf]).