Fig. 1: DNMT3A CHIP monocytes interact with cardiac fibroblasts in healthy and diseased heart. | Nature Communications

Fig. 1: DNMT3A CHIP monocytes interact with cardiac fibroblasts in healthy and diseased heart.

From: DNMT3A clonal hematopoiesis-driver mutations induce cardiac fibrosis by paracrine activation of fibroblasts

Fig. 1

a Schematic representation of the experimental design. Bioinformatic analysis combining monocytes derived from scRNA-seq dataset of PBMC from DNMT3A CHIP and No-CHIP patients, snRNA-seq dataset of cardiac tissue from the septum of control hearts (n = 14 biologically independent samples) and snRNA-seq dataset of cardiac tissue from patients with heart failure with reduced ejection fraction (HFrEF) (n = 3 biologically independent samples) b Uniform manifold approximation and projection (UMAP) plots after integration of monocytes from PBMC and cardiac data sets. The source of data in the integrated object is color coded. c Representation of the different cell type clusters identified after integration d Dot plot of representative marker gene expression in each cell type cluster e Analysis of the integrated objects for cellular interactions by CellChat. Total number of outgoing paracrine signals from monocytes to all cells of the healthy heart is shown. f Analysis of the integrated objects for cellular interactions by CellChat. Total number of outgoing paracrine signals from monocytes to all cells of the HFrEF tissue. g Differential number of outgoing signals enriched in DNMT3A CHIP-carrier monocytes to the individual clusters of cardiac cells of healthy and HFrEF tissues as indicated. FB Fibroblasts. CM Cardiomyocytes. EC Endothelial cells. PC Pericytes. NC Neurons. SMC Smooth muscle cells. Source data are provided as a Source Data file.

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