Related Experiment Video

Updated: Sep 16, 2025

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
10:31

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice

Published on: May 2, 2025

285

CTSS and CD53: Emerging m6A methylation markers in diabetic kidney disease pathogenesis and their clinical

Meng Leilei1, Huang Bin2, Li Rui3

  • 1Department of Pathophysiology, Anhui Medical University, Hefei, 230000, China.

BMC Nephrology
|July 7, 2025
PubMed
Abstract

Insights

This study identifies two N6-methyladenosine (m6A) RNA modification patterns in diabetic kidney disease (DKD), with one linked to increased immune cell infiltration. CTSS and CD53 show potential as clinical biomarkers for DKD.

Area of Science:

  • Molecular Biology
  • Immunology
  • Genomics

Background:

  • Diabetic kidney disease (DKD) is a major global cause of chronic kidney disease (CKD).
  • The role of N6-methyladenosine (m6A) RNA modification in DKD pathogenesis remains unclear.

Purpose of the Study:

  • Investigate m6A RNA modification patterns in DKD.
  • Explore the relationship between m6A patterns and immune regulation in DKD.

Main Methods:

  • Analyzed three GEO datasets for m6A modification patterns.
  • Utilized random forest modeling and consensus clustering for subtype identification.
  • Assessed immune cell infiltration via ssGSEA and validated key genes in mouse models.

Main Results:

  • Identified eight differentially expressed m6A regulators in DKD.
  • Established two distinct m6A modification patterns, one with enhanced immune cell infiltration.
  • Validated CTSS and CD53 as potential biomarkers negatively correlated with glomerular filtration rate.

Conclusions:

  • Revealed two m6A methylation patterns in DKD, one associated with increased immune infiltration.
  • Identified CTSS and CD53 as hub genes with potential as clinical biomarkers for DKD.
Keywords:
BiomarkersDiabetic kidney diseaseImmune microenvironmentRNA modificationm6A

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