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Related Experiment Video

Updated: Sep 11, 2025

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Single-cell transcriptomics combined with spatial transcriptomics reveals a fibrotic microenvironment in

Weili Wang1, Meng Cheng2, Rong Dai2

  • 1First Clinical Medical College, Anhui University of Chinese Medicine, Hefei, China.

European Journal of Pharmacology
|August 15, 2025
PubMed
Summary

Hyperuricemia nephropathy (HN) involves complex cell interactions driving kidney fibrosis. This study identifies heat shock protein beta-1 (Hspb1) and claudin 4 (Cldn4) as key pro-fibrotic factors and potential therapeutic targets.

Keywords:
Hyperuricemia nephropathyIntercellular communicationRenal fibrosisSingle-cell transcriptomicsSpatial transcriptomics

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Genomics

Background:

  • Hyperuricemia nephropathy (HN) is characterized by renal fibrosis, a complex process involving diverse cell types and unclear molecular mechanisms.
  • Understanding the cellular composition and intercellular communication in HN fibrosis is crucial for developing effective treatments.

Purpose of the Study:

  • To elucidate the cellular and molecular mechanisms underlying renal fibrosis in hyperuricemia nephropathy (HN).
  • To identify key cell populations, intercellular interactions, and molecular pathways involved in HN fibrosis.
  • To discover potential therapeutic targets for HN treatment.

Main Methods:

  • Single-cell RNA sequencing and spatial transcriptomics were used to analyze kidney tissues from HN rats.
  • Differential gene expression, pseudotime, gene enrichment, and transcription factor network analyses were performed.
  • In vivo and in vitro experiments validated the roles of identified genes in fibrosis.

Main Results:

  • Identified key cell types including macrophages/monocytes, epithelial cells, and endothelial cells, with macrophages and injured proximal tubular cells crucial to fibrosis.
  • Revealed enhanced macrophage-epithelial interactions and significant involvement of chemokine-mediated signaling pathways (e.g., Ccl4-Ccr5, Ccl3-Ccr5) in HN fibrosis.
  • Identified heat shock protein beta-1 (Hspb1) and claudin 4 (Cldn4) as significantly upregulated pro-fibrotic genes in HN rats, validated through knockdown experiments.

Conclusions:

  • This study uncovers critical cellular and molecular players in HN fibrosis, highlighting the roles of specific cell interactions and signaling pathways.
  • Heat shock protein beta-1 (Hspb1) and claudin 4 (Cldn4) are identified as potential therapeutic targets for HN.
  • The findings offer novel insights into the fibrotic microenvironment in HN, paving the way for new intervention strategies.