Fig. 8: NR4a1 overexpression exacerbates cardiac remodeling and dysfunction in mice that underwent TAC for eight weeks.

A Representative B- and M-mode ultrasound images of AAV9-NC and AAV9-NR4a1 mice 8 weeks after sham or TAC surgery. B Echocardiographic analysis of EF, FS, LVIDd and LVIDs in mice (n = 12); EF: F (3, 44) = 24.81, P = 1.5e-009; FS: F (3, 44) = 13.84, P = 1.7e-006; LVIDd: F (3, 44) = 4.115, P = 1.2e-002; LVIDs: F (3, 44) = 7.995, P = 0.0002. C Representative histopathological cross-sectional images of mouse hearts (scale bar: 2 mm; n = 6). D, E Myocardial hypertrophy was detected by WGA staining and then quantitatively analyzed (scale bar: 50 μm; n = 6); F (3, 20) = 5.364, P = 0.0071. All results are shown as the mean ± SEM, and analysis using one-way ANOVA followed by Bonferroni post hoc test (B and E) was conducted. p values are indicated. Source data are provided as a Source Data file. AAV9, adeno-associated virus 9; TAC, transverse aortic constriction; EF, ejection fractions; FS, fractional shortening; LVIDd, diastolic left ventricular internal diameters; LVIDs, systolic left ventricular internal diameters; WGA, wheat germ agglutinin.