ArticleNature communications2021
An innate contribution of human nicotinic receptor polymorphisms to COPD-like lesions.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Cross-Trait Genome-Wide Association Study Identifies Shared Genetic Architecture Between COPD and Retinal Vascular Phenotypes.International journal of chronic obstructive pulmonary disease · 2026Article
- The role of the gut-lung axis in persistent inflammation and disease progression in chronic obstructive pulmonary disease: mechanistic evidence and therapeutic implications.Frontiers in immunology · 2026Review
- Integrative machine learning and single-cell analysis identifies nicotine-related diagnostic genes and myeloid remodeling in COPD.Frontiers in immunology · 2026Article
- Vaping versus smoking: a quest for long-term impact in a mouse model.BMC pulmonary medicine · 2025Article
- Exploring the Associations BetweenBiomedicines · 2025Article
- Efficient and accurate framework for genome-wide gene-environment interaction analysis in large-scale biobanks.Nature communications · 2025Article
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- The rs16969968 Tobacco Smoking-Related Single-Nucleotide Variant Is Associated with Clinical Markers in Patients with Severe COVID-19.International journal of molecular sciences · 2023Article
- Inference of chronic obstructive pulmonary disease with deep learning on raw spirograms identifies new genetic loci and improves risk models.Nature genetics · 2023Article
- Understanding the habenula: A major node in circuits regulating emotion and motivation.Pharmacological research · 2023Review
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 4 institutions in 4 countries.
Funding
Abstract
Chronic Obstructive Pulmonary Disease is a generally smoking-linked major cause of morbidity and mortality. Genome-wide Association Studies identified a locus including a non-synonymous single nucleotide polymorphism in CHRNA5, rs16969968, encoding the nicotinic acetylcholine receptor α5 subunit, predisposing to both smoking and Chronic Obstructive Pulmonary Disease. Here we report that nasal polyps from rs16969968 non-smoking carriers exhibit airway epithelium remodeling and inflammation. These hallmarks of Chronic Obstructive Pulmonary Disease occur spontaneously in mice expressing human rs16969968. They are significantly amplified after exposure to porcine pancreatic elastase, an emphysema model, and to oxidative stress with a polymorphism-dependent alteration of lung function. Targeted rs16969968 expression in epithelial cells leads to airway remodeling in vivo, increased proliferation and production of pro-inflammatory cytokines through decreased calcium entry and increased adenylyl-cyclase activity. We show that rs16969968 directly contributes to Chronic Obstructive Pulmonary Disease-like lesions, sensitizing the lung to the action of oxidative stress and injury, and represents a therapeutic target.
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What OpenQuestion holds
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.