Fig. 1: Proteome profiling reveals severe mitochondrial dysfunction and impaired oxidative metabolism following myocardial infarction (MI). | Nature Communications

Fig. 1: Proteome profiling reveals severe mitochondrial dysfunction and impaired oxidative metabolism following myocardial infarction (MI).

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

Fig. 1

a Schematic of the study design of Proteome-sequencing, n = 3 mice per group. b Hierarchical clustering of differentially expressed proteins in MI vs. Sham hearts. c Volcano plot displays the fold changes of all detected proteins and p-values in the hearts of mice between the Sham and MI groups, numbers indicate the proteins with expression differences exceeding 1.2-fold. P-values were assessed by a two-sided Student's test. d Gene Ontology (GO) BP terms analysis of differentially expressed proteins in MI vs. Sham hearts, Red, pathways upregulated in MI hearts. Blue, pathways downregulated in the MI heart (Significance was calculated by the hypergeometric test). e Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of differentially expressed proteins in MI vs. Sham hearts, Red, pathways upregulated in MI heart; Blue, pathways downregulated in MI heart (Significance was calculated by hypergeometric test). f Heat map of differentially expressed proteins enriched in pathways related to fatty acid (FA). Each box represents a different animal, with color indicating log2 fold-change. g Pie charts indicating the main subcellular localization of the differentially expressed proteins in MI vs. Sham hearts. h Heat maps of mitochondrial-related protein levels. Each box represents a different animal, with color indicating log2 fold-change.

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