Myocardial‐specific knockdown of Forkhead box protein O6 (FoxO6) improved transverse aortic constriction (TAC)‐induced cardiac function impairment and myocardial fibrosis. (A) Typical western blots indicating FoxO6 in murine myocardium (n = 3−4 mice per group). (B) Typical western blots indicating Kif15 and transforming growth factor‐β1 (TGF‐β1) in murine myocardium (n = 6). (C) Typical images of murine heart sections (after 4 weeks of TAC) stained with Masson's trichrome stain, perivascular area, and interstitial area were, respectively, exhibited. (D) Degree of left ventricular (LV) fibrosis evidenced by collagen volume (n = 7). (E) Typical western blots indicating α‐SMA, collagen I, collagen III, fibronectin, and Postn in murine myocardium (n = 6). (F) Immunostaining of murine myocardium sections to exhibit the expression of α‐SMA (red). (G) Number of α‐SMA‐positive cells (n = 6). (H) Immunostaining of murine myocardium sections to exhibit the expression of vimentin (green) and proliferating cell nuclear antigen (PCNA) (red). (I) Number of vimentin‐ and PCNA‐positive cells (n = 6). (J) Echocardiography of mice. (K) Ejection fraction (EF)% determined via echocardiography (n = 8). 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).