Skip to main content
Fig. 5 | Clinical Epigenetics

Fig. 5

From: Multi-omics integration identifies key upstream regulators of pathomechanisms in hypertrophic cardiomyopathy due to truncating MYBPC3 mutations

Fig. 5

The expression of cell-type-specific markers in 12 cell populations. a The histone acetylation levels of 11 cell-type-specific markers. Each dot represents the average acetylation value of each marker for all samples or only control or HCM samples. One-way ANOVA was used to compare the mean of cardiomyocyte-specific markers with the mean of non-myocyte markers separately: ns (not significant), * P < 0.05, **P < 0.01, *** P < 0.001, **** P < 0.0001. b The mRNA expression levels of 11 cell-type-specific markers. Each dot represents the average expression value of each marker for all samples or only control or HCM samples. One-way ANOVA was used to compare the mean of cardiomyocyte-specific markers with the mean of non-myocyte markers separately: ns (not significant), *P < 0.05, ** P < 0.01, ***P < 0.001, ****P < 0.0001. c Heatmap showing cell-type-specific markers with significantly changed mRNA expression levels in HCM hearts compared to controls. Fold changes of these markers are depicted. Positive fold changes (red) and negative fold changes (blue) represent up-regulation and down-regulation in HCM versus control hearts, respectively. d Histone acetylation levels at the upstream (50 kb) of three cardiomyocytes-specific markers (red) and one T cells-specific marker (violet) were significantly changed between HCM and control hearts. Tracks of one HCM and one control heart were scaled in the UCSC genome browser (ln(x + 1): 0–10). Significantly changed upstream regions are indicated by the black bar above. The transcription start and end site of each marker are indicated by the blue arrow below

Back to article page