FIGURE 5

fabp7a inhibition is sufficient to restore impaired protein homeostasis and decelerate cardiomyocyte senescence in the bag3 cardiomyopathy model. (A–D) Western blot (A) and quantification analysis of LC3II with (B) or without (C) BafA1 treatment, and ubiquitinated protein (D) levels in heart lysates of bag3^e2/e2; fabp7a^e1/+ double‐mutant, bag3^e2/e2, fabp7a^e1/+ single mutant, or WT control fish hearts at 6 months treated with or without 50 nM BafA1 for 4 h. n = 4, one‐way ANOVA. (E, F) Representative images of immunostaining (E) and quantification of the numbers of p16/Mef2 signal (F) in cryosectioned heart tissues co‐stained with anti‐p16 and anti‐Mef2 antibodies. G‐H, Representative images of immunostaining (G) and quantification of the numbers of γH2A.X/α‐actinin signal (H) in cryosectioned heart tissues co‐stained with γH2A.X and anti‐α‐actinin antibodies (G) in bag3^e2/e2; fabp7a^e1/+ double‐mutant, bag3^e2/e2, fabp7a^e1/+ single mutant, or WT control fish hearts at 6 months. Arrows point to overlapping signals. Scale bars: 20 μm. n = 5, one‐way ANOVA. (I–L) Quantitative RT‐PCR analysis of cellular senescence marker p21 and SASP markers in bag3^e2/e2; fabp7a^e1/+ double‐mutant compared to single‐mutant fish and WT control fish hearts at 6 months. n = 3 biological replicates, one‐way ANOVA.