Elevated SLC1A5 links to inflamed endothelial cells and proteinuria in membranous nephropathy patients

Qingqin Tang1, Yi Ling2, Jianzhong Li2

  • 1Center for Clinical Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China.

Peerj
|November 5, 2025
PubMed
Abstract

Insights

This study reveals novel macrophage and endothelial cell interactions in membranous nephropathy (MN). The gene SLC1A5 is identified as a potential biomarker for MN, offering new diagnostic and therapeutic insights.

Area of Science:

  • Nephrology
  • Immunology
  • Genomics

Background:

  • Membranous nephropathy (MN) is an autoimmune glomerular disease causing persistent proteinuria.
  • Understanding MN's complex pathophysiology and signaling is vital for better diagnostics and treatments.

Purpose of the Study:

  • To elucidate the molecular mechanisms and signaling pathways in membranous nephropathy.
  • To identify key cellular players and potential biomarkers for MN progression.

Main Methods:

  • Differential gene expression analysis of MN glomerular transcriptomes.
  • Single-cell, pseudotime, and cell communication analyses to understand MN progression.
  • Mendelian randomization and ELISA for causal relationship and biomarker validation.

Main Results:

  • Identified 95 differentially expressed genes, enriched in immune and metabolic pathways.
  • Highlighted the critical role of macrophage polarization and monocyte/macrophage-endothelial cell interactions.
  • Confirmed SLC1A5 as a key gene causally linked to MN and strongly correlated with proteinuria.

Conclusions:

  • Discovered novel macrophage and endothelial cell subtypes and their interactions in MN.
  • Positioned SLC1A5 as a promising biomarker for MN pathogenesis and progression.

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