Fig. 4: Moderately improved autophagic flux but similar fibrosis and cardiac dysfunction in Tg-ATP6AP2 mice. | Cell Death Discovery

Fig. 4: Moderately improved autophagic flux but similar fibrosis and cardiac dysfunction in Tg-ATP6AP2 mice.

From: ATP6AP2 knockdown in cardiomyocyte deteriorates heart function via compromising autophagic flux and NLRP3 inflammasome activation

Fig. 4

A–C Representative immunoblots and quantitative analysis of whole-cell heart homogenates for ATP6AP2. (n = 4 for each group). Statistical analysis was conducted by the Mann–Whitney test. Quantitative analysis Myh6, Myh7 (D, E) expression of whole-heart homogenates by qRT-PCR. Statistical analysis was conducted by Kruskal–Wallis one-way ANOVA with Dunn post-hoc test. F, G Representative images of echocardiograms and quantitative analysis of LVEF between different groups. Statistical analysis was conducted by Kruskal–Wallis one-way ANOVA with Dunn post-hoc test. H, I Representative hematoxylin and eosin 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. J, K, L Representative immunohistochemical staining and quantitative analysis about staining of ATP6AP2, NLRP3 and immunofluorescence images of SQSTM1/P62. Statistical analysis was conducted by Kruskal–Wallis one-way ANOVA with Dunn post-hoc test. Data were presented as medians and quartiles.

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