Fig. 7: Phenotype changes in shR-ATP6AP2-TAC mice can be partly relieved through blocking NLRP3 inflammasome activation.

C57BL/6 J mice were subjected to TAC, then adenovirus-mediated shR-ATP6AP2 vectors or Scr-control were injected into the tail vein of mice (n = 4 for each group), followed by MCC950 (5 mg/kg/day) or vehicle control. Mice were observed at 28days. A–C Representative images of echocardiograms and quantitative analysis of LVEDD, LVESD between different groups. Statistical analysis was conducted by Kruskal–Wallis one-way ANOVA with Dunn post-hoc test. *P < 0.05 compared with others. D Quantitative analysis of heart weight/body weight ratios (HW/BW; mg/g). Statistical analysis was conducted by Kruskal–Wallis one-way ANOVA with Dunn post-hoc test. *P < 0.05 compared to other groups. E, F Representative images of Masson trichrome staining and quantitative analysis. Statistical analysis was conducted by Kruskal–Wallis one-way ANOVA with Dunn post-hoc test. E, G, H Representative immunohistochemical staining and quantitative analysis of NLRP3, Caspase1 expression. (scale bar = 20 μm). Statistical analysis was conducted by Kruskal–Wallis one-way ANOVA with Dunn post-hoc test. E, I Representative hematoxylin and eosin (HE) staining and quantitative analysis of cardiomyocytes cross-sectional area (scale bar = 20 μm). Statistical analysis was conducted by Kruskal–Wallis one-way ANOVA with Dunn post-hoc test. *P < 0.05 compared with other groups. E, J Representative immunofluorescence images of TUNEL assay showed apoptosis percentage in mouse heart tissues. Statistical analysis was conducted by Kruskal–Wallis one-way ANOVA with Dunn post-hoc test. Data were presented as medians and quartiles.