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

Figure 3.

A multi-panel image displaying various scientific data and analyses. Panels A, B, and C depict dot plots showing levels of calcium ions, ATP, and SDH in different groups. Panel D presents a Western blot image and corresponding expression levels of FDX1 and DLAT proteins. Panel E includes electron microscopy images of mitochondria with percentage damage analysis. Panel F shows HMGB1 levels. Panels G and H illustrate IL-1β and TNF-α levels. Panel I depicts LVEF percentages. Panel J presents LVEDP measurements. Panel K shows NT-proBNP levels. Panel L contains images of heart tissue sections with infarction area analysis. Panel M displays TUNEL and DAPI staining of cells with a bar graph for TUNEL-positive cells. Each graph and image clearly labels three groups: AMI, AMI+NS, and AMI+ATTM.

ATTM inhibits cuproptosis in macrophages, impedes cardiomyocyte apoptosis and relieves HF after AMI in mice. (A-C) Cu2+ level, ATP content, and SDH activity in mouse macrophages determined by kits, n = 12; (D) Levels of cuproptosis-related proteins FDX1 and DLAT in mouse macrophages measured by western blot, n = 12; (E) Mitochondrial damage in cells assessed by TEM; Levels of HMGB1 (F), IL-1β (G), and TNF-α (H) in mouse serum measured by ELISA, n = 12; LVEF (I) and LVEDP (J) detected by echocardiography, n = 12; K, The NT-proBNP level in mouse serum measured by ELISA, n = 12; L, Representative images of TTC-stained heart sections and quantification of myocardial infarction, n = 6; M, Cardiomyocyte apoptosis assessed by TUNEL staining, n = 6. 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.