FIGURE

Figure 2

ID
ZDB-FIG-260111-40
Publication
Xie et al., 2025 - Multi-Omics Integration Identifies TNFRSF1A as a Causal Mediator of Immune Microenvironment Reprogramming in Diabetic Kidney Disease
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Figure 2

Single-cell transcriptomic atlas reveals cellular heterogeneity and disease-specific distribution patterns in control and DKD kidneys: (A) UMAP visualization of tubular epithelial and glomerular cell transcriptomes stratified by disease status (Control vs. DKD). The plot displays the distribution of cell populations in both conditions, with specific cell types annotated including segments of the proximal tubule, loop of Henle, distal tubule, collecting duct, podocytes, parietal epithelial cells, mesangial cells, and endothelial cells within the glomerulus. DKD samples show enrichment of injured proximal tubule cells (iPT) and altered cellular composition compared to controls. (B) UMAP visualization of immune cell transcriptomes in control and DKD kidneys. The plot shows the distribution of various immune cell populations including T cells (CD4+ and CD8+), B cells (naive, memory, and plasma cells), monocytes/macrophages (CD14+ Mono, CD16+ Mono, Mac), neutrophils, NK cells, dendritic cells (cDC, pDC), and proliferating lymphocytes. DKD kidneys exhibit increased monocyte/macrophage infiltration and altered immune cell composition. (C) UMAP visualization of vascular and interstitial cell transcriptomes in control and DKD conditions. The plot displays the distribution of non-immune, non-epithelial stromal populations including peritubular and lymphatic endothelial cells, fibroblast subtypes (Fibroblast_1, Fibroblast_2), myofibroblasts/vascular smooth muscle cells (MyoFib/VSMC), glomerular stromal cells (GS_Stromal), and neural cells.

Expression Data

Expression Detail
Antibody Labeling
Phenotype Data

Phenotype Detail
Acknowledgments
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