Fig. 5: Therapeutic potential of CD36 for infarcted hearts. | Nature Communications

Fig. 5: Therapeutic potential of CD36 for infarcted hearts.

From: Inhibiting CD36 palmitoylation improves cardiac function post-infarction by regulating lipid metabolic homeostasis and autophagy

Fig. 5

a Schematic diagram of the study design, CD36-specific inhibitor Sulfosuccinimidyl oleate sodium (SSO) or solvent once a week intraperitoneally for 4 weeks after MI. Echocardiography was performed at 4 weeks post-MI. b Ejection fraction (EF) and fractional shortening (FS) values were determined to evaluate cardiac function by echocardiography in mice of each group. n = 8 per group. c Averaged infarct size by 2,3,5-triphenyltetrazolium chloride (TTC) staining. n = 5. d, e Histological analysis of myocardial tissue sections with Masson staining (d) and hematoxylin-eosin (H&E) staining (e). n = 6 per group. f Representative transmission electron microscopy images of myocardium from mice with or without SSO treatment after MI. n = 5 per group. g, h Cardiac ceramide (g) and DAG levels (h) after treatment with SSO detected by ELISA assay. n = 8 for ceramide, n = 7 for DAG. i, j Quantitation analysis of Cardiac tissue malondialdehyde (MDA) (i) and superoxide dismutase (SOD) (j) levels. n = 9 per group. Data are presented as means ± SEM. Statistical significance was assessed by Kruskal-Wallis, followed by the false discovery rate [FDR] method of Benjamini and Hochberg test (b, i) and One-way ANOVA, followed by Tukey post hoc multicomparisons test (c, d, g, h and j). Source data are provided as a Source Data file.

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