Figure 1 | Scientific Reports

Figure 1

From: Single-cell sequencing dissects the transcriptional identity of activated fibroblasts and identifies novel persistent distal tubular injury patterns in kidney fibrosis

Figure 1

Ischemia/reperfusion and obstruction induced models of CKD elicit dramatic proximal tubular loss, kidney functional decline and novel cellular clusters. (a) Schemes of injury models (left), macroscopic (middle) and MRI (right) images of normal control, UIR and UUO day 28 kidneys. Kidneys are pointed to with white arrows. R right, L left. (b) Renal blood flow (RBF) at baseline, with vasoconstrictive (PE phenylephrine), vasodilative (SNP sodium nitroprusside) and inotropic agent (DOB dobutamine). Agents administered at 0.1 μl/min/gBW, Ctrl control interval between treatments, n = 3–4 per group, mean ± SD. **P ≤ 0.01, ***P ≤ 0.001, ****P ≤ 0.0001 compared to control, Student’s t test. (c) UMAPs show renal cell populations in the control, UIR and UUO kidneys (n = 3–5 per group). Clusters are distinguished by different colors. PT proximal tubules, S1/2/3 segment 1/2/3, LOH loop of Henle, DT distal tubule, CD-P collecting duct principal, CD-I collecting duct intercalated, Podo podocytes, Endo endothelial, Macro macrophages, Neutro neutrophils, cDC conventional dendritic cells, NK natural killer, prTcell proliferating Tcell, Fibro fibroblasts, frTEC failed repair tubular epithelial cells.

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