Figure 1.

Resistin inhibition attenuates TAC-induced hypertrophy, cardiac dysfunction, and fibrosis in RKO mice. (A) Study protocol for TAC induction in WT or RKO mice. (B) Gravimetric analysis of heart weight/body weight (left panel; n = 7–8), heart weight/tibia length (middle panel; n = 7–8), and lung weight/tibia length (right panel; n = 5) in WT and RKO mice subjected to sham or TAC for 10 weeks. (C) Representative images of Masson’s trichrome (top panels, scale bar, 2 mm) and WGA (lower panels, scale bar, 100 µm, n = 60) stained hearts sections; quantification of cardiomyocytes cross-sectional area. (D) Real-time PCR analysis of the expression levels of Anf, Myh7, Myh6, and Acta1 (n = 4). (E) Representative echocardiographic images; quantification of fractional shortening and LVIDs of WT or RKO mice subjected to sham or TAC for 10 weeks (n = 7–8). (F) Assessment of the load-independent parameter ESPVR by pressure–volume conductance catheters (n = 4). (G) Survival curve of WT or RKO mice subjected to sham or pressure overloaded 10 weeks post-TAC (n = 7–14). (H) Representative images of Masson’s trichrome-stained hearts sections and cardiac fibrosis quantification as percentage of blue stained area vs. control (scale bar, 100 µm) in the indicated groups of mice (n = 4). Real-time PCR analysis of the expression levels of Col1a1, FN, CCN2, and LOX (n = 4). N, each animal is shown as an individual point whereas horizontal lines represent median values. Values are shown as mean ± S.E.M. with each experiment performed in biological and technical replicates as indicated. Significance was evaluated by Student’s t-test or one-way ANOVA with Tukey’s post-hoc test. P values <0.05 were considered significant.