Identification of Disulfidptosis-Related Genes and Molecular Subgroups in Rheumatoid Arthritis for Diagnostic Model and Patient Stratification

  • 0Department of Rheumatology and Immunology, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, People's Republic of China.

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Summary

This summary is machine-generated.

This study identifies four key genes linking disulfidptosis, a novel cell death pathway, to rheumatoid arthritis (RA). A diagnostic model and patient stratification based on these genes offer new insights for RA assessment.

Area Of Science

  • Immunology
  • Cell Biology
  • Genetics

Background

  • Rheumatoid arthritis (RA) pathogenesis involves complex cell death pathways.
  • Disulfidptosis, characterized by disulfide bond accumulation, is a newly identified cell death mechanism.
  • The specific role of disulfidptosis in RA pathogenesis remains largely unexplored.

Purpose Of The Study

  • To investigate the association between disulfidptosis and rheumatoid arthritis.
  • To identify key genes involved in disulfidptosis relevant to RA.
  • To develop a diagnostic model and patient stratification for RA based on these genes.

Main Methods

  • Utilized weighted gene co-expression network analysis (WGCNA) and differential gene expression analysis on public RA datasets.
  • Employed machine learning algorithms to identify hub genes associated with RA and disulfidptosis.
  • Constructed a diagnostic model using nomograms and ROC curves; performed consensus clustering for patient stratification.

Main Results

  • Identified four hub genes (KLHL2, POLK, CLEC4D, NXT2) significantly upregulated in RA patients.
  • Validated a diagnostic model with superior performance compared to individual genes.
  • Discovered two RA subtypes with distinct clinical and immunological profiles based on hub gene expression.

Conclusions

  • Four hub genes provide novel insights into disulfidptosis in RA.
  • The developed diagnostic model and patient stratification aid in assessing RA risk and disease activity.