Fig. 2: GCN5 overexpression accelerates pressure overload-induced cardiac hypertrophy and dysfunction. | Cell Death & Disease

Fig. 2: GCN5 overexpression accelerates pressure overload-induced cardiac hypertrophy and dysfunction.

From: GCN5-mediated regulation of pathological cardiac hypertrophy via activation of the TAK1-JNK/p38 signaling pathway

Fig. 2: GCN5 overexpression accelerates pressure overload-induced cardiac hypertrophy and dysfunction.

A–D Echocardiographic assessment of EF, FS, LVEDd, and LVESd values in GCN5-overexpressing mice and control mice subjected to sham or TAC surgery at 4 weeks (n = 10–12 mice/group). E–G HW/BW, HW/TL, and LW/BW ratios in GCN5-overexpressing mice and control mice subjected to sham or TAC surgery at 4 weeks (n = 10–12 mice/group). H Representative images of heart sections stained with H&E and WGA to analyze heart and cardiomyocyte size, respectively (n = 5 mice/group). I Representative images of heart sections stained with Masson’s trichrome stain to analyze perivascular and interstitial fibrotic area (n = 5 mice/group). J Effects of GCN5 overexpression on the mRNA levels of the hypertrophic marker genes and fibrotic marker genes in the hearts of mice subjected to sham or TAC surgery at 4 weeks (n = 5–7 mice/group, ∗∗P < 0.01 vs SHAM, #P < 0.05 vs AAV9-Vector TAC 4 W, ##P < 0.01 vs AAV9-Vector TAC 4 W). Data are shown as the mean ± SD from three independent experiments.

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