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Related Experiment Video

Updated: Jan 20, 2026

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GSTO1 as a Potential Risk Factor for Diabetic Nephropathy: Evidence From Mendelian Randomisation and Multi-Omics

Jiang Tan1, Sisi Lei2, Liang Zhao3

  • 1College of Artificial Intelligence Medicine, Chongqing Medical University, Chongqing, China.

Nephrology (Carlton, Vic.)
|January 19, 2026
PubMed
Summary
This summary is machine-generated.

Glutathione S-transferase omega 1 (GSTO1) genetic variants are linked to increased diabetic nephropathy (DN) risk. Upregulated GSTO1 expression in kidney cells suggests it may play a causal role in DN development.

Keywords:
GSTO1Mendelian randomisationdiabetic nephropathy

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Area of Science:

  • Nephrology
  • Genetics
  • Molecular Biology

Background:

  • Diabetic nephropathy (DN) is a primary cause of end-stage renal disease (ESRD).
  • The role of Glutathione S-transferase omega 1 (GSTO1) in DN pathogenesis is not fully understood.
  • GSTO1 is involved in cellular redox regulation and inflammatory processes.

Purpose of the Study:

  • To investigate the potential causal relationship between GSTO1 and the risk of developing DN.
  • To explore GSTO1 expression patterns in DN.
  • To determine if GSTO1 could be a therapeutic target for DN.

Main Methods:

  • Two-sample Mendelian randomization (MR) analysis using genetic variants associated with GSTO1.
  • Analysis of GSTO1 expression in kidney tissues and cells using public databases (Nephroseq, GEO) and single-cell RNA sequencing (scRNA-seq).
  • In vitro experiments assessing GSTO1 expression in HK-2 cells exposed to high glucose.

Main Results:

  • MR analysis indicated a significant association between GSTO1 genetic variants and increased DN risk.
  • GSTO1 expression was found to be elevated in DN patient samples across multiple datasets.
  • Increased GSTO1 expression was observed in proximal tubular cells and in high-glucose treated kidney cells.

Conclusions:

  • Preliminary evidence suggests a potential causal link between GSTO1 and DN.
  • GSTO1 may contribute to the pathogenesis of diabetic nephropathy.
  • GSTO1 warrants further investigation as a potential biomarker and therapeutic target for DN.