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Oxidative Phosphorylation Pathway in Ankylosing Spondylitis: Multi-Omics Analysis and Machine Learning.

Yuling Chen1, Yuan Xu2, Shuangyan Cao1

  • 1Department of Rheumatology and Immunology, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, China.

International Journal of Rheumatic Diseases
|April 29, 2025
PubMed
Summary

This study reveals mitochondrial oxidative phosphorylation (OXPHOS) is dysregulated in ankylosing spondylitis (AS), identifying LAMTOR2 as a key gene. This finding offers potential new therapeutic targets for AS precision medicine.

Keywords:
ScRNA‐seqankylosing spondylitismachine learningoxidative phosphorylation

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Area of Science:

  • Immunology
  • Genetics
  • Metabolomics

Background:

  • Ankylosing spondylitis (AS) is a chronic inflammatory disease impacting the axial skeleton.
  • Immune dysregulation and elevated cytokines (TNF-α, IL-17) characterize AS.
  • Mitochondrial oxidative phosphorylation (OXPHOS) is critical for immune cell function and implicated in AS.

Purpose of the Study:

  • To explore OXPHOS-related mechanisms in AS pathogenesis.
  • To identify key genes and potential therapeutic targets using machine learning.
  • To advance precision medicine approaches for AS treatment.

Main Methods:

  • Analysis of peripheral blood mononuclear cells (PBMCs) transcriptomic and scRNA-seq data from AS patients.
  • Weighted gene co-expression network analysis (WGCNA) to identify OXPHOS-associated gene modules.
  • Machine learning (SVM-RFE, Random Forest, LASSO) and RT-PCR for gene identification and validation.

Main Results:

  • OXPHOS pathway significantly distinguishes AS patients from controls.
  • Elevated OXPHOS scores observed in AS patients' dendritic cells and monocytes.
  • Identified LAMTOR2, APBB1IP, and DGKQ as hub genes; LAMTOR2 showed higher expression in AS and promotes TH17 cell differentiation.

Conclusions:

  • Multi-omics data reveal a critical interplay between OXPHOS and AS.
  • LAMTOR2 emerges as a promising therapeutic target for ankylosing spondylitis.
  • Findings contribute to understanding AS mechanisms and developing precision medicine strategies.