Fig. 8: Inhibition of CD36 palmitoylation attenuates cardiac dysfunction after MI.

a Schematic diagram of the study design, CD36 knockout (CD36KO) mice were injected with adenoassociated virus 9 (AAV9)–cTnT (cardiac troponin T2)-WT-CD36 (wildtype CD36) or AAV9-cTNT-AA-SS-CD36 (CD36 with mutated palmitoylation sites) via the tail vein. After 4 weeks, the mice underwent left anterior descending coronary artery ligation surgery, followed by echocardiographic measurements on cardiac function. b Protein levels of CD36 in total homogenates and different fractions of WT-CD36 and AA-SS-CD36 mice. n = 6 for total CD36; n = 4 for surface membrane CD36.; n = 8 for subcellular CD36. c–e Echocardiography determined EF and FS values to assess cardiac function after sham or LAD surgery in WT-CD36 and AA-SS-CD36 mice. n = 7 per group. f–h Histological sections with hematoxylin-eosin (H&E) staining and Masson staining of myocardial tissues from WT-CD36 and AA-SS-CD36 mice. n = 5 per group. i Representative transmission electron microscopy images of cardiac tissues from WT-CD36 and AA-SS-CD36 mice (yellow arrow indicates autophagosome). n = 5 per group. j–m Changes in cardiac biomarker levels: cardiac ceramide (j), DAG (k), malondialdehyde (MDA) (l) and superoxide dismutase (SOD) (m) levels in WT-CD36 and AA-SS-CD36 mice. n = 10 for ceramide; n = 8 for DAG; n = 9 for MDA and SOD. Data are presented as means ± SEM. Statistical significance was assessed by One-way ANOVA, followed by Tukey post hoc multicomparisons test (b–g and k) and Kruskal-Wallis, followed by the false discovery rate [FDR] method of Benjamini and Hochberg test (j, l and m). Source data are provided as a Source Data file.