Figure 7: Cardioprotective Effect of the ATM Inhibitor on Ang II–Induced Pathological Cardiac Remodeling

(A) Timeline of Ang II infusion and ATM inhibitor (KU55933) or vehicle administration in mice. (B) The ratio of HW/TL in WT and HMGB1-Tg mice subjected to Ang II infusion and vehicle or ATM inhibitor (KU55933) treatment (n = 8 in WT vehicle group; n = 8 in WT Ang II + vehicle group; n = 6 in HMGB1-Tg Ang II + vehicle group; n = 6 in WT Ang II + KU55933 group; n = 6 in HMGB1-Tg Ang II + KU55933 group). (C) Analysis of CM cross-sectional area by H&E staining in left ventricular sections in WT and HMGB1-Tg mice subjected to Ang II infusion and vehicle or ATM inhibitor (KU55933) treatment (n = 10 in WT vehicle group; n = 10 in WT Ang II + vehicle group; n = 9 in HMGB1-Tg Ang II + vehicle group; n = 7 in WT Ang II + KU55933 group; n = 9 in HMGB1-Tg Ang II + KU55933 group). (D) Analysis of cardiac fibrosis by Masson’s trichrome staining in left ventricular sections in WT and HMGB1-Tg mice subjected to Ang II infusion and vehicle or ATM inhibitor (KU55933) treatment (n = 6 per group). (E) Representative images of CM cross-sectional area by H&E staining (Scale bars = 20 μm) and cardiac fibrosis by Masson’s trichrome staining (Scale bars = 50 μm) in left ventricular sections in WT and HMGB1-Tg mice subjected to Ang II infusion and vehicle or ATM inhibitor (KU55933) treatment. Results are presented as the mean ± SE. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001. Abbreviations as in Figures 1, 2, 3, 4, 5, and 6.