Fig. 1: Cardiac-specific CPT2 deletion disrupts mitochondrial FAO.

a The role of CPT1 located on the OMM and CPT2 on the IMM in transporting LCFA in the form of Acyl-CoA into the mitochondrial matrix for FAO. b Western blot analysis and (c) quantification of CPT2 expression in heart tissue derived from wild-type and CPT2^H-KO mice (n  =  4). Data represent mean ± s.d. GAPDH is shown as a loading control. d–f Lipidomic profiles of wild-type and CPT2^H-KO hearts (n  =  5). d Heatmap illustrating hierarchical clustering of differential features detected from wild-type and CPT2^H-KO cardiac samples run in duplicate by liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based lipidomic analysis. Normalized peak intensities were clustered in two dimensions based on Euclidean distance (column, samples; row, metabolites). Colors indicate the metabolite abundances. Higher and lower values are colored red and blue, respectively. Total lipid metabolite profiling in mouse hearts derived from wild-type and CPT2^H-KO was assessed by principle-component analysis (PCA) (e) and Mummichog pathway analysis (f). All the matched pathways are displayed as circles. The color and size of each circle are based on the P-value (one-sided), determined by the Mummichog algorithm. g Relative fold change profile of acyl-carnitines in hearts from wild-type and CPT2^H-KO mice. Acylcarnitines, classified by the number of carbon atoms and double bonds in their acyl chains, are listed on the Y-axis. Data on the X-axis represent the mean fold change ± s.d. (CPT2^H-KO/wild-type, n  =  5). The P-values were calculated using an unpaired two-tailed Student’s t test (c, g). Source data are provided as a Source Data file.