ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2021
Aryl hydrocarbon receptor deficiency causes the development of chronic obstructive pulmonary disease through the integration of multiple pathogenic mechanisms.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Aryl hydrocarbon receptor pharmacology-mechanisms, ligands, and therapeutic potential.Pharmacological reviews · 2026Review
- AhR as a Common Denominator in Immunity and Inflammation in Chronic Lung Diseases: Molecular and Clinical Insights.Diseases (Basel, Switzerland) · 2026Review
- Compartmental analysis of the pulmonary proteome reveals novel functions of the aryl hydrocarbon receptor.Respiratory research · 2026Article
- The Role of Aryl Hydrocarbon Receptor in Airway Remodeling: Mechanistic Insights Across Cellular Functions.Clinical reviews in allergy & immunology · 2026Review
- Activation of aryl hydrocarbon receptor by cigarette smoke induces oxidative stress, autophagy impairment and cellular senescence.Tobacco induced diseases · 2026Article
- Article
- The AhR Is a Critical Regulator of the Pulmonary Response to Cannabis Smoke.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Decreased Aryl Hydrocarbon Receptor Gene Expression and Polymorphic Variants Association with Increase COPD Risk.International journal of chronic obstructive pulmonary disease · 2025Article
- Aryl Hydrocarbon Receptor Activation in Pulmonary Alveolar Epithelial Cells Limits Inflammation and Preserves Lung Epithelial Cell Integrity.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Assessment of wood smoke induced pulmonary toxicity in normal- and chronic bronchitis-like bronchial and alveolar lung mucosa models at air-liquid interface.Respiratory research · 2024Article
- SNPs Sets in Codifying Genes for Xenobiotics-Processing Enzymes Are Associated with COPD Secondary to Biomass-Burning Smoke.Current issues in molecular biology · 2023Article
- Insight into the pulmonary molecular toxicity of heated tobacco products using human bronchial and alveolar mucosa models at air-liquid interface.Scientific reports · 2022Article
- Standardized Cannabis Smoke Extract Induces Inflammation in Human Lung Fibroblasts.Frontiers in pharmacology · 2022Article
- Article
- Aryl Hydrocarbon Receptor Defect Attenuates Mitogen-Activated Signaling through Leucine-Rich Repeats and Immunoglobulin-like Domains 1 (LRIG1)-Dependent EGFR Degradation.International journal of molecular sciences · 2021Article
- Differential Regulation of the Asthmatic Phenotype by the Aryl Hydrocarbon Receptor.Frontiers in physiology · 2021Article
- The Aryl Hydrocarbon Receptor Suppresses Chronic Smoke-Induced Pulmonary Inflammation.Frontiers in toxicology · 2021Article
- Caffeine Therapy for Apnea of Prematurity: Role of the CircadianFrontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
25 authors at 13 institutions in 4 countries.
Funding
Abstract
Emphysema, a component of chronic obstructive pulmonary disease (COPD), is characterized by irreversible alveolar destruction that results in a progressive decline in lung function. This alveolar destruction is caused by cigarette smoke, the most important risk factor for COPD. Only 15%-20% of smokers develop COPD, suggesting that unknown factors contribute to disease pathogenesis. We postulate that the aryl hydrocarbon receptor (AHR), a receptor/transcription factor highly expressed in the lungs, may be a new susceptibility factor whose expression protects against COPD. Here, we report that Ahr-deficient mice chronically exposed to cigarette smoke develop airspace enlargement concomitant with a decline in lung function. Chronic cigarette smoke exposure also increased cleaved caspase-3, lowered SOD2 expression, and altered MMP9 and TIMP-1 levels in Ahr-deficient mice. We also show that people with COPD have reduced expression of pulmonary and systemic AHR, with systemic AHR mRNA levels positively correlating with lung function. Systemic AHR was also lower in never-smokers with COPD. Thus, AHR expression protects against the development of COPD by controlling interrelated mechanisms involved in the pathogenesis of this disease. This study identifies the AHR as a new, central player in the homeostatic maintenance of lung health, providing a foundation for the AHR as a novel therapeutic target and/or predictive biomarker in chronic lung disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.