Evidence map›Paper›PMID 27713627›Full record

ArticleInternational journal of chronic obstructive pulmonary disease2016

Elevated circulating PAI-1 levels are related to lung function decline, systemic inflammation, and small airway obstruction in chronic obstructive pulmonary disease.

Hao Wang, Ting Yang, Diandian Li, Yanqiu Wu, Xue Zhang, Caishuang Pang, Junlong Zhang, Binwu Ying, Tao Wang, Fuqiang Wen

Open access · goldAbstract read
In one paragraph

Article in International journal of chronic obstructive pulmonary disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 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

10 authors at 2 institutions in 1 country.

Hao WangDepartment of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China; Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Ting YangDepartment of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China; Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Diandian LiDepartment of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China; Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Yanqiu WuDepartment of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China; Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Xue ZhangDepartment of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China; Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Caishuang PangDepartment of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China; Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Junlong ZhangDepartment of Laboratory Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Binwu YingDepartment of Laboratory Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Tao WangDepartment of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China; Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Fuqiang WenDepartment of Respiratory and Critical Care Medicine, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China; Division of Pulmonary Diseases, State Key Laboratory of Biotherapy of China, West China Hospital of Sichuan University, Chengdu, Sichuan, People's Republic of China.
Sichuan University · CNWest China Hospital of Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPlasminogen activator inhibitor-1 (PAI-1) and soluble urokinase-type plasminogen activator receptor (suPAR) participate in inflammation and tissue remolding in various diseases, but their roles in chronic obstructive pulmonary disease (COPD) are not yet clear. This study aimed to investigate if PAI-1 and suPAR were involved in systemic inflammation and small airway obstruction (SAO) in COPD.

methodsDemographic and clinical characteristics, spirometry examination, and blood samples were obtained from 84 COPD patients and 51 healthy volunteers. Serum concentrations of PAI-1, suPAR, tissue inhibitor of metalloproteinase-1 (TIMP-1), Matrix metalloproteinase-9 (MMP-9), and C-reactive protein (CRP) were detected with Magnetic Luminex Screening Assay. Differences between groups were statistically analyzed using one-way analysis of variance or chi-square test. Pearson's partial correlation test (adjusted for age, sex, body mass index, cigarette status, and passive smoke exposure) and multivariable linear analysis were used to explore the relationships between circulating PAI-1 and indicators of COPD.

resultsFirst, we found that serum PAI-1 levels but not suPAR levels were significantly increased in COPD patients compared with healthy volunteers (125.56±51.74 ng/mL versus 102.98±36.62 ng/mL,

conclusionOur findings first illustrate that elevated serum PAI-1 levels are related to the lung function decline, systemic inflammation, and SAO in COPD, suggesting that PAI-1 may play critical roles in the pathogenesis of COPD.

Indexed as

AgedAirway ObstructionBiomarkersCase-Control StudiesChi-Square DistributionC-Reactive ProteinDisease ProgressionFemaleForced Expiratory VolumeHumansInflammation MediatorsLinear ModelsLungMaleMatrix Metalloproteinase 9Middle AgedBiomarkersC-Reactive ProteinInflammation MediatorsMatrix Metalloproteinase 9MMP9 protein, humanPlasminogen Activator Inhibitor 1PLAUR protein, humanReceptors, Urokinase Plasminogen ActivatorSERPINE1 protein, humanTIMP1 protein, humanTissue Inhibitor of Metalloproteinase-1chronic obstructive pulmonary disease (COPD)plasminogen activator inhibitor-1 (PAI-1)small airway obstruction (SAO)systemic inflammation

Identifiers

PMID27713627
PMCPMC5044991
OpenAlexW2524132196

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.