Evidence map›Paper›PMID 31297601›Full record

ArticleLung2019

A Polymorphism rs6726395 in Nrf2 Contributes to the Development of Emphysema-Associated Age in Smokers Without COPD.

A Sugitani, K Asai, T Watanabe, T Suzumura, K Kojima, H Kubo, K Sato, N Ijiri, K Yamada, T Kimura and 3 more

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Lung, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 43% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 4 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 1 institution in 1 country.

A SugitaniDepartment of Respiratory Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan.
K AsaiDepartment of Respiratory Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan. kazuasai@med.osaka-cu.ac.jp.ORCID 0000-0001-8400-863X
T WatanabeDepartment of Respiratory Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan.
T SuzumuraDepartment of Respiratory Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan.
K KojimaDepartment of Respiratory Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan.
H KuboDepartment of Respiratory Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan.
K SatoDepartment of Respiratory Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan.
N IjiriDepartment of Respiratory Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan.
K YamadaDepartment of Respiratory Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan.
T KimuraDepartment of Premier Preventive Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan.
S FukumotoDepartment of Premier Preventive Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan.
K HirataDepartment of Respiratory Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan.
T KawaguchiDepartment of Respiratory Medicine, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Osaka City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionSeveral studies have reported that single nucleotide polymorphisms (SNPs) in the gene encoding NF-E2-related factor 2 (Nrf2) contribute to airflow limitations in smokers without COPD. Although small airway lesions and emphysema contribute cooperatively to airflow limitation, the relationship between Nrf2 SNPs and the development of emphysema in smokers without COPD is not well understood.

methodsHealthy subjects who underwent an annual health checkup with computed tomography (CT) of the chest at Osaka City University Hospital were prospectively recruited. The percentage of low-attenuation area (%LAA) on chest CT was quantified, and correlations between %LAA, Nrf2 SNP [rs6726395 (G/A)] genotypes, and clinical characteristics were examined.

resultsA total of 245 subjects without COPD [non-/light-smoker: 153 (62.4%) and smoker: 92 (37.6%)] were enrolled. The %LAA in the upper lung field was higher than that in the lower lung field (p < 0.001). The %LAA in smokers was significantly higher than that in non-/light-smokers (p = 0.021). The %LAA showed significant but weak correlation with age in all subjects (r = 0.141, p = 0.028). Divided by genotype, the %LAA of the upper lung field was significantly correlated with age in smokers with genotype GG (wild type) (r = 0.333, p = 0.022), but was not significantly correlated with age in smokers with genotype AG/AA. These correlations were not observed in non-/light smokers.

conclusionA polymorphism rs6726395 in Nrf2 can contribute to the development of emphysema-associated aging in smokers. The Nrf2 SNP may be a predictive factor for smoking-induced emphysema, and genotyping of Nrf2 SNP may serve as biomarker for emphysema prevention.

Indexed as

Polymorphism, Single NucleotideSmokersAdultAgedAge FactorsFemaleGenetic Predisposition to DiseaseHeterozygoteHomozygoteHumansJapanLungMaleMiddle AgedNF-E2-Related Factor 2Non-SmokersNFE2L2 protein, humanNF-E2-Related Factor 2COPDEmphysemaNF-E2-related factor2Percentage of low-attenuation areaSingle nucleotide polymorphism

Identifiers

PMID31297601
OpenAlexW2956699548

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

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.