Evidence map›Paper›PMID 28356730›Full record

ArticleInternational journal of chronic obstructive pulmonary disease2017

Plasminogen activator inhibitor-1 is elevated in patients with COPD independent of metabolic and cardiovascular function.

Benjamin Waschki, Henrik Watz, Olaf Holz, Helgo Magnussen, Beata Olejnicka, Tobias Welte, Klaus F Rabe, Sabina Janciauskiene

Open access · goldAbstract read
In one paragraph

Article in International journal of chronic obstructive pulmonary disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
2.7field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Review
  7. Small airway fibroblasts from patients with chronic obstructive pulmonary disease exhibit cellular senescence.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
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  14. Review
  15. Interrelations between COVID-19 and other disorders.Clinical immunology (Orlando, Fla.) · 2021
    Review
  16. Lrp1 Regulation of Pulmonary Function. Follow-Up of Human GWAS in Mice.American journal of respiratory cell and molecular biology · 2021
    Article
  17. Article
  18. Article
  19. Vitamin DEBioMedicine · 2019
    Article
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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

8 authors at 3 institutions in 1 country.

Benjamin WaschkiPneumology, LungenClinic Grosshansdorf, Grosshansdorf, Germany; Pulmonary Research Institute at LungenClinic Grosshansdorf, Grosshansdorf, Germany; Airway Research Center North (ARCN), German Center for Lung Research (DZL), Grosshansdorf, Germany.
Henrik WatzPulmonary Research Institute at LungenClinic Grosshansdorf, Grosshansdorf, Germany; Airway Research Center North (ARCN), German Center for Lung Research (DZL), Grosshansdorf, Germany.
Olaf HolzFraunhofer Institute for Toxicology and Experimental Medicine, Hannover, Germany; Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), German Center for Lung Research (DZL), Hannover, Germany.
Helgo MagnussenPulmonary Research Institute at LungenClinic Grosshansdorf, Grosshansdorf, Germany; Airway Research Center North (ARCN), German Center for Lung Research (DZL), Grosshansdorf, Germany.
Beata OlejnickaDepartment of Medicine, Trelleborg Hospital, Trelleborg, Sweden.
Tobias WelteBiomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), German Center for Lung Research (DZL), Hannover, Germany; Department of Respiratory Medicine, Hannover Medical School, Hannover, Germany.
Klaus F RabePneumology, LungenClinic Grosshansdorf, Grosshansdorf, Germany; Airway Research Center North (ARCN), German Center for Lung Research (DZL), Grosshansdorf, Germany.
Sabina JanciauskieneBiomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), German Center for Lung Research (DZL), Hannover, Germany; Department of Respiratory Medicine, Hannover Medical School, Hannover, Germany.
LungenClinic Grosshansdorf · DEMedizinische Hochschule Hannover · DEFraunhofer Institute for Toxicology and Experimental Medicine · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionPlasminogen activator inhibitor-1 (PAI-1), a major inhibitor of fibrinolysis, is associated with thrombosis, obesity, insulin resistance, dyslipidemia, and premature aging, which all are coexisting conditions of chronic obstructive pulmonary disease (COPD). The role of PAI-1 in COPD with respect to metabolic and cardiovascular functions is unclear.

methodsIn this study, which was nested within a prospective cohort study, the serum levels of PAI-1 were cross-sectionally measured in 74 stable COPD patients (Global Initiative for Chronic Obstructive Lung Disease [GOLD] Stages I-IV) and 18 controls without lung disease. In addition, triglycerides, high-density lipoprotein cholesterol, fasting plasma glucose, waist circumference, blood pressure, smoking status, high-sensitive C-reactive protein (hs-CRP), adiponectin, ankle-brachial index, N-terminal pro-B-type natriuretic peptide, and history of comorbidities were also determined.

resultsThe serum levels of PAI-1 were significantly higher in COPD patients than in controls, independent of a broad spectrum of possible confounders including metabolic and cardiovascular dysfunction. A multivariate regression analysis revealed triglyceride and hs-CRP levels to be the best predictors of PAI-1 within COPD. GOLD Stages II and III remained independently associated with higher PAI-1 levels in a final regression analysis.

conclusionThe data from the present study showed that the serum levels of PAI-1 are higher in patients with COPD and that moderate-to-severe airflow limitation, hypertriglyceridemia, and systemic inflammation are independent predictors of an elevated PAI-1 level. PAI-1 may be a potential biomarker candidate for COPD-specific and extra-pulmonary manifestations.

Indexed as

AgedBiomarkersCardiovascular SystemCase-Control StudiesChi-Square DistributionC-Reactive ProteinCross-Sectional StudiesFemaleHumansHypertriglyceridemiaInflammationInflammation MediatorsLinear ModelsLungMaleMiddle AgedBiomarkersC-Reactive ProteinInflammation MediatorsPlasminogen Activator Inhibitor 1SERPINE1 protein, humanTriglyceridesankle-brachial indexcardiovascular diseasechronic obstructive pulmonary diseasehypertriglyceridemiainflammationN-terminal pro-B-type natriuretic peptideplasminogen activator inhibitor-1

Identifiers

PMID28356730
PMCPMC5367764
OpenAlexW2603815916

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.