Fig. 4

CYP2E1 enhances susceptibility to pathological cardiac remodeling induced by ISO treatment. (A) Schematic representation of pathological cardiac hypertrophy stimulation and the experimental strategy in myocardium-specific Cyp2e1-KO and Cyp2e1-OV rats. (B) Transthoracic echocardiographic images (M-mode) illustrating left ventricle (LV) morphology in six groups: control-saline, Cyp2e1-OV-saline, Cyp2e1-KO-saline, control-ISO, Cyp2e1-OV-ISO (OV-ISO), and Cyp2e1-KO-ISO (KO-ISO). (C-J) Echocardiographic parameters, including LVPWs, LVPWd, LVAWs, LVAWd, LVIDs, LVIDd, ejection fraction, and fractional shortening, were analyzed across the six groups. Data are presented as mean ± SEM; n = 6–13 rats per group. (K-L) Representative images of whole-heart transverse sections and magnified view of the left ventricle with H&E staining. scale bars: blue = 5 mm; black = 40 μm. (M) Myocardial fiber morphology in myocardial tissue was assessed using immunofluorescence staining with wheat germ agglutinin (green). Paraffin sections were imaged using a confocal microscope. DAPI (blue) indicates nuclei. Scale bars: white = 40 μm. (N) Quantification of cross-sectional cardiomyocyte area across the six groups. Data shown are mean ± SEM; n = 3 rats and 54 cardiomyocytes per group. Multiple comparisons between groups were executed using ANOVA with Tukey correction. *P < 0.05, **P < 0.01, ***P < 0.001