Evidence map›Paper›PMID 25369941›Full record

ArticleBMC pulmonary medicine2014

Genetic variants in ADAM33 are associated with airway inflammation and lung function in COPD.

Xinyan Wang, Wan Li, Kun Huang, Xiaowen Kang, Zhaoguo Li, Chengcheng Yang, Xiaomei Wu, Lina Chen

Open access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 30% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. T1 polymorphism in a disintegrin and metalloproteinase 33 (ADAM33) gene may contribute to the risk of childhood asthma in Asians.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017
    Pooled it
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  8. The etiologic origins for chronic obstructive pulmonary disease.International journal of chronic obstructive pulmonary disease · 2019
    Review
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

8 authors at 2 institutions in 1 country.

Xinyan Wang
Wan Li
Kun Huang
Xiaowen Kang
Zhaoguo Li
Chengcheng Yang
Xiaomei WuDepartment of Respiratory, the Second Affiliated Hospital of Harbin Medical University, Harbin 150081, China. wu.xiaomei@hotmail.com.
Lina Chen
Harbin Medical University · CNSecond Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenetic factors play a role in the development and severity of chronic obstructive pulmonary disease (COPD). The pathogenesis of COPD is a multifactorial process including an inflammatory cell profile. Recent studies revealed that single nucleotide polymorphisms (SNPs) within ADAM33 increased the susceptibility to COPD through changing the airway inflammatory process and lung function.

methodsIn this paper, we investigated associations of four polymorphisms (T1, T2, S2 and Q-1) of ADAM33 as well as their haplotypes with pulmonary function and airway inflammatory process in an East Asian population of patients with COPD.

resultsWe found that T1, T2 and Q-1 were significantly associated with the changes of pulmonary function and components of cells in sputum of COPD, and T1 and Q-1 were significantly associated with cytokines and mediators of inflammation in airway of COPD in recessive models. 10 haplotypes were significantly associated with transfer factor of the lung for carbon monoxide in the disease state, 4 haplotypes were significantly associated with forced expiratory volume in one second, and other haplotypes were associated with airway inflammation.

conclusionsWe confirmed for the first time that ADAM33 was involved in the pathogenesis of COPD by affecting airway inflammation and immune response in an East Asian population. Our results made the genetic background of COPD, a common and disabling disease, more apparent, which would supply genetic support for the study of the mechanism, classification and treatment for this disease.

Indexed as

HaplotypesADAM ProteinsAgedAsia, EasternAsian PeopleFemaleForced Expiratory VolumeHumansInflammation MediatorsInterleukin-6Interleukin-8Lymphocyte CountMacrophagesMaleMiddle AgedPolymorphism, Single NucleotideADAM33 protein, humanADAM ProteinsInflammation MediatorsInterleukin-6Interleukin-8Tumor Necrosis Factor-alphaVascular Endothelial Growth Factor A

Identifiers

PMID25369941
PMCPMC4228268
OpenAlexW2051969893

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.