Figure 3: ANGPTL2-overexpressing mice are predisposed to HF.

(a) Shown are representative M-mode echocardiography recordings (top row), HE-stained sections of heart mid-portion (second row, Scale bar, 1 mm), gross appearance of whole heart (third row) and lung (fourth row) and sections of Masson’s Trichrome-stained heart tissue (bottom row, Scale bar, 100 μm) from αMHC-Angptl2 Tg and WT littermate mice 3 weeks after TAC or sham surgery. Ruler tick marks represent 1 mm. (b–e) Comparison of heart tissue from αMHC-Angptl2 Tg and WT littermate mice 3 weeks after TAC or sham surgery. (b) FS (%), reduction percentage of FS (%), and LVID;d. (c) Heart weight per body weight (HW/BW) ratio and lung weight per body weight (LW/BW) ratio. (d) Percentage of fibrosis area. (e) Relative expression of genes associated with HF and cardiac fibrosis. WT values were set to 1. n=6–10 per group. (f) ATP levels in hearts of αMHC-Angptl2 Tg and WT mice 3 weeks after TAC or sham surgery. n=6–11 per group. (g) Kaplan–Meier curve analysis following TAC surgery in αMHC-Angptl2 Tg (n=13) compared with WT (n=28) mice. P<0.001 between genotypes by log-rank test. (h) Representative M-mode echocardiography recordings (left), %FS (middle) and percent reduction of FS (right) in αMHC-Angptl2 Tg and WT littermate mice 2 weeks after Ang II or vehicle treatment (n=4–5 per group). (i) HW/BW ratio from αMHC-Angptl2 Tg and littermate mice 2 weeks after Ang II or vehicle treatment (n=4–5 per group). (j) Relative expression of markers of HF and cardiac fibrosis in heart of αMHC-Angptl2 Tg and WT littermate mice 2 weeks after Ang II or vehicle treatment (n=4–5 per group). Levels seen in vehicle-treated WT mice were set to 1. Data are means±s.e.m. Statistical significance was determined by Student’s t test (c–f,i,j, percent reduction of FS in b and h, and LVID;d in b) or two-way ANOVA (%FS in b and h). *P<0.05, **P<0.01, ^†P<0.001 between genotypes or groups.