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Related Concept Videos

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Related Experiment Video

Updated: Apr 21, 2026

Isolation, Characterization, And High Throughput Extracellular Flux Analysis of Mouse Primary Renal Tubular Epithelial Cells
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Single-Cell Transcriptomic Atlas Reveals Metabolic Reprogramming and Transdifferentiation Trajectories in Tubular

Xinhui Mao1, Minggang Wei2, Yilin Li3

  • 1Nephrology Department, Baoying County People's Hospital, No.1 Xincheng Road Baoying County, Yangzhou, Jiangsu, 225800, China.

International Journal of Genomics
|April 20, 2026
PubMed
Summary

Chronic kidney disease (CKD) involves tubular cell changes. This study reveals cellular diversity and metabolic shifts in CKD tubular cells, identifying potential therapeutic targets for kidney function preservation.

Keywords:
chronic kidney diseasemetabolic reprogrammingproximal tubule heterogeneitysingle-cell RNA sequencingtubular epithelial cells

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Genomics

Background:

  • Chronic kidney disease (CKD) is characterized by tubular epithelial cell dysfunction and fibrosis.
  • The cellular heterogeneity and molecular drivers of CKD progression remain incompletely understood.
  • Understanding tubular cell diversity is crucial for developing precision medicine therapies for CKD.

Purpose of the Study:

  • To characterize the cellular heterogeneity and metabolic states of tubular epithelial cells in CKD patients.
  • To identify molecular mechanisms underlying tubular cell dysfunction and transdifferentiation in CKD.
  • To reveal potential therapeutic targets for preserving kidney function in CKD.

Main Methods:

  • Single-cell RNA sequencing was performed on renal cells from CKD patients, focusing on tubular epithelial populations.
  • Unsupervised clustering, metabolic pathway scoring, and pseudotemporal trajectory inference were employed.
  • Machine learning classification was used to analyze cell subsets and segment-specific markers.

Main Results:

  • Tubular cells exhibited significant heterogeneity and a metabolic shift from oxidative phosphorylation to glycolysis.
  • Distinct cell clusters were identified: OXPHOS-high, glycolytic, dormant, and intermediate states.
  • Pseudotemporal analysis revealed progressive cellular transitions driven by genes like MALAT1 and ANXA1, with proximal tubule cells showing diverse transcriptomic signatures.

Conclusions:

  • This study provides a molecular atlas of tubular epithelial cell heterogeneity in CKD.
  • Metabolic reprogramming and transdifferentiation are key drivers of tubular dysfunction and fibrosis in CKD.
  • The findings highlight potential therapeutic targets for retaining tubular function and mitigating CKD progression.