Fig. 6: Molecular characterization of fibroblasts in the cardiac organoids.
From: Modeling cardiac fibroblast heterogeneity from human pluripotent stem cell-derived epicardial cells
A UMAP dimensionality reduction of fibroblasts in control and  CI samples. B Relative frequency of each fibroblast cluster in control and CI samples. C Heatmap depicting the top 30 genes in each fibroblast cluster (logFC threshold = 0.3, min.pct = 0.3, adjusted p-value < 0.05). Color bars indicate cluster (top) and condition (bottom). Differential expression was performed using the Wilcoxon Rank Sum Test (unpaired, two-sided), and p-values were adjusted for multiple comparisons using Bonferroni correction. D Pathway enrichment analysis (gProfiler, GO: Biological Processes) was performed using DEGs upregulated in CI vs. control in each fibroblast cluster. Heatmap depicting the enrichment score (−log10 of adjusted p-value) scaled across clusters for each pathway individually. E Violin plots showing expression of fibrosis-related genes (FAP, LTBP2, PRRX1, MEOX1) in each fibroblast cluster in the control and CI samples. F Violin plots showing expression of proteoglycan-related genes (BGN, LUM, MGP, PGN, VCAN, ASPN) in each fibroblast cluster in the control and CI samples. G An in vivo human heart failure signature was generated using the top 25 DEGs upregulated in cardiac fibroblasts in coronary heart failure vs. normal hearts (single cell dataset published in Wang et al.). Each cell in all fibroblast clusters of control and CI organoids was scored using this signature and displayed in the heatmap. A two-sided unpaired t-test was performed for each pairwise comparison (cardiac injury vs. control in each cluster). ****p<0.0001, ***p<0.001, **p<0.01, *p<0.05.
