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Figure 5. Cardiomyocyte overexpression of lnc-mg improves cardiac contractile function and attenuates myocardial remodeling after myocardial infarction. (A) Schematic of the mouse MI model, AAV9-mediated lnc-mg overexpression, and experimental timeline. Created in BioRender. Jia S, (2026) https://BioRender.com/6ylhd7s. (B) RT-qPCR validation of lnc-mg overexpression at 7 days post-MI (7 dpi). Eight independent mice were analyzed per treatment group (n = 8 biological replicates per group). (C-E) Representative M-mode echocardiographic images (C) and serial measurements of LVEF (D) and LVFS (E) from 7 to 56 days post-MI. The same cohort of mice was followed throughout the study (n = 8 mice per treatment group). Each mouse represented an independent biological replicate, and measurements obtained from the same mouse at different time points were treated as repeated measurements. (F and G) Representative serial transverse Masson’s trichrome-stained heart sections collected at 56 days post-MI from the ligation site to the apex, with quantification of the scar circumference ratio at the mid-ventricular level (G). Sections from three independent mice were analyzed per treatment group (n = 3 biological replicates per group). Scale bar, 500 μm. (H and I) Myostation analysis of contractile force in left ventricular myocardial strips under graded electrical stimulation (5-10 V) (H) and increasing extracellular Ca²⁺ concentrations (1.5-7.5 mM) (I) at 56 days post-MI. Myocardial strips were obtained from six independent mice per treatment group (n = 6 biological replicates per group), with the mouse serving as the experimental unit. Measurements obtained from the same myocardial preparation at different stimulation voltages or Ca²⁺ concentrations were treated as repeated measurements. Data are presented as mean ± SEM. *P < 0.05; **P < 0.01; ****P < 0.0001.