Journal: Frontiers in Immunology

Article Title: SLC31A1 knockdown mitigates post-MI heart failure via regulation of copper metabolism

doi: 10.3389/fimmu.2026.1707203

Figure Lengend Snippet: 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.

Article Snippet: The suspension was probed with antibodies against allophycocyanin-conjugated F4/80 (1:100, E-AB-F0995E, Elabscience Biotechnology Co., Ltd., Wuhan, Hubei, China) and fluorescein isothiocyanate (FITC)-conjugated CD11b (1:100, E-AB-F1081C, Elabscience) in the dark at 4°C for 30–40 min.

Techniques: Enzyme-linked Immunosorbent Assay, Staining, TUNEL Assay, Flow Cytometry, Expressing, Quantitative RT-PCR, Western Blot, Standard Deviation