Cardiac‐specific knockout of Forkhead box protein O6 (FoxO6) inhibited angiotensin‐II (Ang‐II)‐induced cardiac fibrosis. (A) Lung‐to‐body weight (LW/BW) ratio of mice (n = 5 mice per group). (B) Echocardiography of mice. (C–E) Left ventricular ejection fraction (LVEF), fraction shortening (FS)%, and left ventricle volume (LV vol) determined using echocardiography (n = 8). (F) Typical images of murine heart sections stained with Masson's trichrome stain, perivascular area, and interstitial area were amplified. (G) Degree of left ventricular (LV) fibrosis evidenced by collagen volume (n = 7). (H) Typical western blots indicating transforming growth factor‐β1 (TGF‐β1), α‐SMA, collagen I, fibronectin, and Postn in murine myocardium. (I) Cardiac protein expression levels of TGF‐β1, α‐SMA, collagen I, fibronectin, and Postn in murine myocardium (n = 6). (J) Cardiac mRNA expression levels of genes encoding fibrotic markers TGF‐β1, α‐SMA, collagen I, collagen III, and Postn in each group (n = 6). (K) Immunostaining of murine myocardium sections to exhibit the expression of α‐SMA (red). (L) Number of α‐SMA‐positive cells (n = 6). (M) Immunostaining of murine myocardium sections to exhibit the expression of vimentin (green) and proliferating cell nuclear antigen (PCNA) (red). (N) Number of vimentin‐ and PCNA‐positive cells (n = 6). Data were analyzed by one‐way analysis of variance (ANOVA). *
p < 0.05, **
p < 0.01, ***
p < 0.001, ****
p < 0.0001. Statistics are carried out as mean ± standard deviation (SD).