Fig. 2: General autophagy and mitophagy are transiently upregulated in hypertrophic hearts but are decreased during decompensated heart failure combined with NLRP3 inflammasome upregulation. | Cell Death Discovery

Fig. 2: General autophagy and mitophagy are transiently upregulated in hypertrophic hearts but are decreased during decompensated heart failure combined with NLRP3 inflammasome upregulation.

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

Fig. 2

Representative immunoblots and quantitative analysis of LC3A/B and P62/SQSTM1, Atg5 (A, B), PINK1 (C), ATP6AP2, NLRP3, pro-caspase1 (D) are shown from whole-cell heart homogenates (n = 5 for each group). Statistical analysis was conducted by Kruskal–Wallis one-way ANOVA with Dunn post-hoc test. For LC3AB: *P < 0.05 vs. sham-operated mice. For P62/SQSTM1: #P < 0.05 vs. sham-operated mice. For Atg5: &P < 0.05 vs. sham-operated mice. At least four independent experiments were conducted. E Representative immunoblots for autophagic flux measure of whole-cell heart homogenates for LC3AB with or without BafA1. F, G Quantitative analysis of ELISA measurement of serum levels of IL-1β, TNF-α expression levels. Statistical analysis was conducted by Kruskal–Wallis one-way ANOVA with Dunn post-hoc test. Data were presented as medians and quartiles. H Representative immunohistochemical staining of ATP6AP2, NLRP3, Caspase1, IL-1β, IL-18 in sham groups, TAC5day, TAC56day.(scale bar = 20 μm). I, J Representative immunofluorescence images of colocalization of NLRP3 with ATP6AP2 or SQSTM1/P2, with NLRP3 in tissue section.

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