Fig. 4.

Cardiac-specific deletion of MAO-A increases myocardium catecholamine contents and enhances contractile function. A Quantitative measurements of endogenous NE in mouse heart, plasma, and brain (n ≥ 6 mice per group). B Quantification of cyclic AMP levels in MAO-A-FF and CKO heart tissues (n = 8 FF, 7 CKO). C Quantification of ROS in mice hearts (n = 10 mice per group). D Heart weight/body weight ratio in MAO-A-FF and CKO hearts. n = 8. E, F Western blots show the phosphorylation of PLB (p-Ser16), TnI (p-Ser23/24), RyR2 (p-Ser2808), and LTCC (p-Ser1928) in MAO-A-FF and CKO heart tissues (n = 6/group). G Schematic shows that deletion of MAO-A enhances local β₁AR signaling at the SR but not PM microdomain. H M-mode echocardiography was recorded for 2 min at baselines and for 8 min after each drug administration. The maximal cardiac response was reported. Representative echocardiography images of MAO-A-FF and CKO mice before and after EPI and DOB stimulation (100 µg/kg, i.p.). I Quantification of EF and HR before and after EPI or DOB stimulation n = 9. Data are shown as mean ± SD. p values were obtained by unpaired Student’s t test (A–D, and F) or one-way ANOVA with Tukey’s multiple comparison correction