fig5

Immunometabolic drivers of renal fibrosis and potential therapeutic targets in diabetic kidney disease

Figure 5. Single-cell transcriptomic landscape and cell-type-specific expression validation of DKD-associated causal proteins. (A and B) UMAP plots of single-cell transcriptomes integrated from DKD and normal kidney samples, colored by unsupervised clusters (A) and sample group (B); (C) Circle packing visualization showing the annotation of major cell lineages, including T cells, B cells, epithelial cells, fibroblasts, macrophages, and mixed cells; (D) Stacked bar plot representing the relative proportion of each cell type in DKD vs. normal tissues; (E) Aggregate expression levels of candidate genes (CSTA, LYZ, and TGFBI) comparing DKD and normal groups across all cells; (F) Feature plots illustrating the spatial distribution and abundance of CSTA, LYZ, and TGFBI on the UMAP embedding, split by condition; (G-I) Cell-type-specific differential expression analysis of CSTA (G), LYZ (H), and TGFBI (I). Box plots display the normalized expression levels in DKD (blue) and normal (red) groups across identified cell types. Statistical significance was determined using the Wilcoxon rank-sum test (*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001; ns, not significant). DKD: Diabetic kidney disease; UMAP: uniform manifold approximation and projection; CSTA: cystatin A; LYZ: lysozyme; TGFBI: transforming growth factor beta induced.

Metabolism and Target Organ Damage
ISSN 2769-6375 (Online)
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