ArticleInternational journal of chronic obstructive pulmonary disease2025
Decreased Aryl Hydrocarbon Receptor Gene Expression and Polymorphic Variants Association with Increase COPD Risk.
Article in International journal of chronic obstructive pulmonary disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- AhR as a Common Denominator in Immunity and Inflammation in Chronic Lung Diseases: Molecular and Clinical Insights.Diseases (Basel, Switzerland) · 2026Review
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Authors and funding
8 authors.
Funding
Abstract
Background: The Aryl Hydrocarbon Receptor (AHR) is a ligand-activated transcription factor that regulates gene expression, including those involved in metabolizing xenobiotic chemicals. The association of AHR with the onset and severity of Chronic Obstructive Pulmonary Disease (COPD) has not yet been elucidated. This study aimed to investigate the correlation between two AHR polymorphisms and the expression levels of this gene in COPD patients compared to healthy controls. Methods: The AHR gene expression level and frequency of two polymorphisms, rs2066853 and rs2074113, were studied in 154 COPD patients and 145 healthy individuals using RT-PCR and AS-PCR methods respectively. Results: The findings showed a significant difference in the frequencies of G and A, as well as GG and GA genotypes in rs2066853 between patients and healthy controls [G: OR: 0.4, CI: 0.24-0.67, (p=0.0002); A: OR: 2.44, CI: 1.48-4.03, (p=0.0002); genotypes GG: OR: 0.37, CI: 0.21-0.65, (p=0.0002) and GA: OR: 2.42, CI: 1.40-4.18 (p=0.001)]. Additionally, the GT genotype frequency in the rs2074113 was different between two groups [GT: OR: 0.23, CI: 0.07-0.72, (p=0.008)]. Moreover, AHR gene expression was significantly lower in COPD patients compared to healthy controls (P=0.03). Noteworthy, individuals with the GA genotype in rs2066853 exhibited lower AHR expression levels than those with the GG genotype. Conclusion: The presence of allele A and the GA genotype of the rs2066853 polymorphism in the AHR gene is significantly associated with COPD, suggesting a genetic predisposition. Moreover, reduced AHR expression in patients supports its key role in COPD pathogenesis.
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