Abstract: FR-PO360
A Human Single-Cell Transcriptomic Atlas Characterizes the Kidney in Diabetic Kidney Disease
Session Information
- Diabetic Kidney Disease: Basic - I
November 03, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Diabetic Kidney Disease
- 701 Diabetic Kidney Disease: Basic
Authors
- Lv, Zhimei, Shandong Provincial Hospital, Jinan, Shandong, China
- Hu, Jinxiu, Shandong Provincial Hospital, Jinan, Shandong, China
- Wang, Rong, Shandong Provincial Hospital, Jinan, Shandong, China
Background
Diabetic kidney disease (DKD), a common and devastating microvascular complication of diabetes, is the leading cause of end-stage renal disease (ESRD). However, the mechanisms of kidney injury in DKD are largely unknown.
Methods
To elucidate the heterogeneity and the underlying mechanisms for DKD progression, we performed single-cell RNA sequencing (scRNA-seq) on human kidneys collected from 3 DKD and 3 normal samples using 10× Genomics.
Results
A total of 51315 cells were enrolled for analyses, and nine kidney cell types and seven immune cell types were identified. The cell-type-specific changes in gene expression and signaling pathways of podocytes, fibroblasts, endothelial cells, proximal tubules and macrophages indicate abnormal regulation associated with inflammation, apoptosis, oxidative stress, extracellular matrix accumulation, fibrosis and immune activation. In particular, we show that podocytes and proximal tubules have a tremendous capacity to regenerate, which is involved in the repair of injury. Extracellular vesicles, important mediators of intercellular communication, might play vital roles in this process. In addition, we identified new candidate transcription factors responsible for the progression of DKD. We also revealed an M1-M2 hybrid pattern, in which M1 and M2 are coupled for activation in macrophages in DKD. Furthermore, we observed an increased intercellular interaction among podocytes, fibroblasts, endothelial cells, proximal tubules, and macrophages in DKD.
Conclusion
Our study advances the understanding of DKD pathogenesis and provides novel therapeutic targets for its treatment in the future.