Fig 2: Up-Regulation of YAP Contributes to the Development of Cardiac Dysfunction in Response to Pressure Overload in the Presence of HFD(A) Schematic representation of the experimental protocol. In B–D, mice were fed with either ND or HFD for 8 weeks. Four weeks after the start of ND or HFD, mice were subjected to either sham operation or transverse aortic constriction (TAC) for 4 weeks (4w). (B) Time course of percent fractional shortening (%FS) and left ventricular end-diastolic dimension (LVEDD) evaluated with echocardiography (n = 6, each). (C) Left ventricular end-diastolic pressure (LVEDP) and pressure gradient, evaluated by hemodynamic measurements (n = 6, each). (D) Kaplan-Meier survival curves after TAC. (E) Representative gel pictures of YAP, TEAD1, OSM, MYH7, ACTA2, RUNX1, and α-tubulin in the heart (n = 6, each). All results are mean ± SEM. *p < 0.05 by analysis of variance. Abbreviations as in Figure 1.

Fig 3: Verteporfin Improves Pressure Overload–Induced Cardiac Hypertrophy in the Presence of HFD(A) Schematic representation of the experimental protocol. Mice were fed with either ND or HFD for 8 weeks. Four weeks after the start of ND or HFD, mice were subjected to either sham operation or TAC in the presence or absence of verteporfin for 4 weeks. (B) Kaplan-Meier survival curves for HFD-fed mice after TAC in the presence or absence of verteporfin. (C) %FS and LVEDD evaluated with echocardiography 4 weeks after TAC, with or without verteporfin treatment (n = 6, each). (D) Left ventricular weight to tibial length (LV W/ TL) ratio (n = 6, each). (E) Lung weight to tibial length (Lung W/ TL) ratio (n = 6, each). (F) Representative gel pictures of YAP, TEAD1, OSM, MYH7, ACTA2, RUNX1, and α-tubulin in the heart (n = 6, each). All results are mean ± SEM. *p < 0.05, **p < 0.01 by analysis of variance. i.p. = intraperitoneal; N.S. = not significant; Op = operation; post op = postoperative; other abbreviations as in Figures 1 and 2.