Effect and Mechanism of LRP6 on Cardiac Myocyte Ferroptosis in Myocardial Infarction

Figure 1

Ferroptosis inhibitor improves the pathological process of MI. (a, b) The LVEF% and LVFS% in both the MI group and the control group. Time stamp: 200 ms; scale bar: 1 mm. Pooled data: biological replication indicated five mice in each group. Data were compared with ctrl by one-way analysis of variance (ANOVA) with Bonferroni’s post hoc test. (c) Cardiomyocytes’ death were stained with H&E in the sham group, the MI+NS group, and the MI+Fer-1 group. Scale bar: 50 μm. The presented images were representative. (d) Evaluation of MDA and Fe²⁺ levels in infarcted myocardial tissue. Upper: MDA level; bottom: Fe²⁺ level. Pooled data: biological replication indicated five mice in each group. (e) Effect of Fer-1 mediated the viability of cardiomyocytes treated with erastin, ZVAD-FMK, or necrosulfonamide. Pooled data: biological replication indicated five mice in each group. Data were and compared with ctrl by one-way ANOVA with Bonferroni’s post hoc test.

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