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. 2019 Oct 4;116(10):1742–1755. doi: 10.1093/cvr/cvz251

Figure 5.

Figure 5

Cardiac-specific Trx1 heterozygous knockout mice are susceptible to pressure overload (PO)-induced heart failure. Pressure overload was applied to mice at 3–9 months of age (Wild: 5.5 ± 2.0, Wild TAC: 6.1 ± 0.9, Trx1cKO: 5.6 ± 1.4, Trx1cKO TAC: 5.9 ± 1.2) (A) Ejection fraction, (B) lung congestion, (C) cardiomyocyte cell size, (D) cardiac fibrosis, and (E) apoptotic cell death were examined in hetero Trx1cKO mice under PO conditions. (F) Increased Prdx1 with sulphonic acid formation in hetero Trx1cKO mice under PO conditions. (G) Downregulation of mitochondrial proteins in hetero Trx1cKO mice under PO conditions. (H) The level of LC3-II and p62 was evaluated with immunoblot analyses. The numbers of mice examined in each experimental group were: 5–8 (A), 5–6 (B), 5–6 (C), 5 (D), and 5–6(E–G). Statistical significance was determined with the Student’s t test (B, D, E, and F) and one-way ANOVA followed by Tukey test (A, C, G, and H). *P<0.05, **P<0.01, and ***P<0.001.