Fig. 3
From: Single-cell transcriptomics reveals common epithelial response patterns in human acute kidney injury
AKI leads to depletion of differentiated cell states and enrichment of “New” cell states within the kidney epithelium. A, B UMAP plot of subclustered kidney tubular epithelial cells (A) and their enrichment or depletion in AKI based on statistical testing of relative abundances within the respective major cell type (B) (see the “Methods” section for details). In A, cellular subtypes of the kidney tubule are annotated as indicated. To enhance visibility, color code is indicated below the respective labeling. In B, the same UMAP plot as in A is color-coded based on enrichment (red) or depletion (blue) in AKI individuals. C, D Analogous plots for subclustering of endothelial cells (ECs). Please note the emergence of one AKI-associated subcluster, EC-New 1. E, F Analogous plots for subclusterings of interstitial cells. PT-S1-3, PT S1-3 segments; c/mTAL, cortical/medullary TAL; TL, DTL, thin limb and descending thin limb; CCD, OMCD, IMCD, cortical/outer and inner medullary collecting duct principal cell; lymphEC, lymphatic EC; GEC, glomerular EC; FenEC 1–4, fenestrated endothelial cell types; DVR, descending vasa recta; MC, mesangial cells; VSMC, vascular smooth muscle cells; REN, renin-transcribing cells; Fibro, fibroblasts; NEUR, neuronal cells