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Screening and Preliminary Validation of Parthanatos-Related Key Genes in Asthma Using Transcriptomic and Machine

Jiawei Zhao1, Danni Li2, Chunli Yang3

  • 1Department of Pediatrics, The Fifth Affiliated Hospital of Dali University (Baoshan People's hospital), Baoshan, People's Republic of China.

Journal of Inflammation Research
|March 25, 2026
PubMed
Summary

This study identifies ANXA3, CEACAM6, and CRISP3 as key genes in parthanatos-related programmed cell death in asthma. These findings offer a foundation for understanding asthma mechanisms and developing diagnostics.

Keywords:
asthmaenrichment analysisimmune infiltrationkey genesparthanatos

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Area of Science:

  • Molecular Biology
  • Immunology
  • Genetics

Background:

  • Parthanatos, a programmed cell death pathway mediated by Poly polymerase 1, is poorly understood in asthma.
  • Identifying key molecular players in asthma pathogenesis is crucial for developing effective treatments.

Purpose of the Study:

  • To integrate transcriptomic data with parthanatos-related genes (PRGs) to identify key molecular players in asthma.
  • To explore the role of parthanatos in asthma pathogenesis.

Main Methods:

  • Utilized public asthma datasets (GSE69683, GSE134544) for analysis.
  • Employed differential expression analysis, weighted gene co-expression network analysis (WGCNA), and machine learning.
  • Performed immune infiltration analysis and predictive modeling for environmental compound interactions.

Main Results:

  • Prioritized three genes: ANXA3, CEACAM6, and CRISP3, linked to inflammatory and metabolic pathways.
  • Observed significant immune cell disparities between asthmatic and control groups.
  • Identified potential therapeutic targets and validated CEACAM6 and CRISP3 upregulation in asthmatic blood samples.

Conclusions:

  • Identified ANXA3, CEACAM6, and CRISP3 as preliminarily validated parthanatos-related key genes in asthma.
  • Established a foundational gene signature for future asthma research.
  • Highlighted the clinical relevance of these genes in respiratory diseases.