Fig. 4: Comparison of cardiac gene expressions of control, WT-TAC and KO-TAC mice.
a, Principal component analysis (PCA) visualization showing global gene expression in WT control, WT-TAC and KO-TAC mice (n = 3 each). b, Heat map showing the expression levels of differentially expressed genes in WT control, WT-TAC and KO-TAC mice. Left: differentially expressed genes in WT and WT-TAC mice. Right: differentially expressed genes between the WT-TAC and KO-TAC mice. c, GO analysis of differentially expressed genes. Genes were upregulated in WT-TAC mice compared with those in WT control mice. The red bars indicate GO terms associated with genes expressed in cardiomyocytes. The white bars represent other GO terms not specifically related to cardiomyocyte-expressed genes. d, GO analysis of differentially expressed genes. Genes were downregulated in KO-TAC mice compared with those in WT-TAC mice. The red bars indicate GO terms associated with genes expressed in cardiomyocytes. The white bars represent other GO terms not specifically related to cardiomyocyte-expressed genes. e, Top: GSEA of genes associated with MYC targets. Plots were prepared using the HALLMARK_MYC_TARGETS_V1 dataset (containing genes regulated by MYC) from the Molecular Signatures Database54. Bottom: GSEA of genes associated with the cardiac hypertrophy pathway. P values were derived from one-sided permutation tests with FDR correction. f, GSEA of genes associated with fibrosis. Genes associated with fibrosis were upregulated in WT-TAC mice compared with those in WT control mice. P values were derived from one-sided permutation tests with FDR correction. g, GSEA of genes associated with fibrosis. Genes associated with fibrosis were not significantly different between the KO and WT-TAC mice. P values were derived from one-sided permutation tests with FDR correction.
