Fig. 9: Insights into the role of CD36 palmitoylation in cardiomyocyte autophagy through PGAM5.

a Western blotting analysis of LC3II and SQSTM1 protein levels in myocardium from WT-CD36 and AA-SS-CD36 mice. n = 7. b Western blotting analysis of LC3II and SQSTM1 protein levels in cardiomyocytes transfected with WT-CD36 or AA-SS-CD36 for 48 h. n = 10. c Overlap between CD36 binding proteins, as assessed by CoIP-MS analysis and proteins in the Autophagy Database (http://autophagy.info/). d Endogenous CD36 immunoprecipitation followed by anti-CD36 and anti-PGAM5 western blot analysis of cardiomyocytes (NMVCs). n = 4. e Quantification of Cyto-ID staining in cardiomyocytes (NMVCs) transfected with WT-CD36 or AA-SS-CD36 for 48 h, and then treated with 500 nM rapamycin (Rapa) and 60 µM CQ, the combination for 16 h. n = 6 per group. f–h Western blotting analysis of the mitochondria expression of CD36 and PGAM5 in cardiomyocytes (NMVCs) transfected with WT-CD36 or AA-SS-CD36. n = 7 per group. i Relative PGAM5 mRNA levels in cardiomyocytes transfected with WT-CD36 or AA-SS-CD36 for 48 h. n = 5. j Time course of PGAM5 protein stability in cardiomyocytes (NMVCs) transfected with WT-CD36 or AA-SS-CD36 after treatment with CHX (10 µg/ml). n = 6. k Ubiquitination of exogenous PGAM5 in cardiomyocytes (NMVCs) transfected with WT-CD36 or AA-SS-CD36. Data are representative of six independent experiments. l The mitochondria expression of phosphorylation Fundc1 and total Fundc1 protein in cardiomyocytes (NMVCs) transfected with WT-CD36 or AA-SS-CD36. n = 6 for phosphorylation Fundc1; n = 7 for total Fundc1. Data are presented as means ± SEM. Statistical significance was assessed by Kruskal-Wallis, followed by false discovery rate [FDR] method of Benjamini and Hochberg test (a), two-tailed unpaired Student t test (b, d, g, i and l), two-way ANOVA, followed by Tukey post hoc multicomparisons test (e, j) and two-tailed Mann-Whitney U test (h). Source data are provided as a Source Data file.