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. 2026 Feb 23;17:1707203. doi: 10.3389/fimmu.2026.1707203

Figure 1.

Graphs and images present experimental data on cardiac function and tissue analysis. A-C show bar graphs comparing LVEF, LVEDP, and NT-proBNP levels across groups: Sham, AMI, AMI+sh-NC, and AMI+sh-SLC31A1. D depicts heart sections stained to highlight infarction areas, with a graph comparing percentage infarction. E includes tunel and DAPI staining with a graph of tunel-positive cells. F presents flow cytometry data with cell populations highlighted. G shows relative SLC31A1 expression in a bar graph. H displays a Western blot of SLC31A1 with a corresponding expression analysis graph. Statistical significance is marked by asterisks.

SLC31A1 is abundantly expressed in post-AMI HF mouse models, silencing of which mitigates post-AMI HF by inhibiting cardiomyocyte apoptosis. (A, B) LVEF and LVEDP detected by echocardiography, n = 12; (C) The serum NT-proBNP level measured by ELISA, n = 12; (D) Representative images of TTC-stained heart sections and quantification of myocardial infarction, n = 6; (E) Cardiomyocyte apoptosis assessed by TUNEL staining, n = 6; (F) Sorting of macrophages (F4/80+/CD11b+) by flow cytometry; (G) mRNA expression of SLC31A1 determined by RT-qPCR, n = 12; (H) The level of SLC31A1 protein determined by western blot, n = 3. Data were described as mean ± standard deviation, with multi-group comparisons conducted by one-way ANOVA, followed by Tukey’s post hoc tests. *p < 0.05, **p < 0.01, ***p < 0.001.