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<p>This study investigates genes linking oxidative stress to idiopathic pulmonary fibrosis (IPF) through multi-omics data integration. We collected oxidative stress-related genes from GeneCards and integrated data for gene expression (eQTLs), DNA methylation (mQTLs), and protein expression (pQTLs). Genome-wide association study (GWAS) data on IPF from Allen et al. served as the discovery set, with FinnGen R10 for validation. Summary data-based Mendelian randomization (SMR) and colocalization analyses assessed interactions and shared causal variants, followed by multi-omics integration with tissue-specific validation. SMR and colocalization screening identified 90 mQTLs, 15 eQTLs, and 2 pQTLs (<i>KRT18</i> and <i>FOXO1</i>) linked to IPF in the discovery cohort. Twelve mQTLs were validated in the FinnGen cohort, with <i>MUC1</i> showing strong SMR and colocalization evidence (eQTL). Multi-omics integration validated <i>NDUFA9</i> (mQTL-eQTL) level and <i>FOXO1</i> (mQTL-eQTL-pQTL). Our study identified key oxidative stress-related genes (i.e., <i>FOXO1</i> and <i>NDUFA9</i>) in IPF pathogenesis, highlighting the need for further research to inform prevention and treatment.</p>

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Investigating the potential of oxidative stress-related gene as predictive markers in idiopathic pulmonary fibrosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月1日

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  • Yuhao Wang,
  • Zhao Zhang,
  • Hongnan Zhang,
  • Luyao Xu,
  • Shuling Huang,
  • Ying Wen,
  • Zhiming Zhuang,
  • Xiaoxin Li,
  • Jinyi Lu,
  • Xudong Li

摘要

This study investigates genes linking oxidative stress to idiopathic pulmonary fibrosis (IPF) through multi-omics data integration. We collected oxidative stress-related genes from GeneCards and integrated data for gene expression (eQTLs), DNA methylation (mQTLs), and protein expression (pQTLs). Genome-wide association study (GWAS) data on IPF from Allen et al. served as the discovery set, with FinnGen R10 for validation. Summary data-based Mendelian randomization (SMR) and colocalization analyses assessed interactions and shared causal variants, followed by multi-omics integration with tissue-specific validation. SMR and colocalization screening identified 90 mQTLs, 15 eQTLs, and 2 pQTLs (KRT18 and FOXO1) linked to IPF in the discovery cohort. Twelve mQTLs were validated in the FinnGen cohort, with MUC1 showing strong SMR and colocalization evidence (eQTL). Multi-omics integration validated NDUFA9 (mQTL-eQTL) level and FOXO1 (mQTL-eQTL-pQTL). Our study identified key oxidative stress-related genes (i.e., FOXO1 and NDUFA9) in IPF pathogenesis, highlighting the need for further research to inform prevention and treatment.