Evidence map›Paper›PMID 27163696›Full record

ArticlePloS one2016

Role of HIF1A, VEGFA and VEGFR2 SNPs in the Susceptibility and Progression of COPD in a Spanish Population.

Rebeca Baz-Dávila, Adriana Espinoza-Jiménez, María Del Cristo Rodríguez-Pérez, Javier Zulueta, Nerea Varo, Ángela Montejo, Delia Almeida-González, Armando Aguirre-Jaime, Elizabeth Córdoba-Lanús, Ciro Casanova

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Bioscience reports · 2018
    Trial
  2. International journal of chronic obstructive pulmonary disease · 2026
    Article
  3. Does Chronic Obstructive Pulmonary Disease Originate from Different Cell Types?American journal of respiratory cell and molecular biology · 2023
    Article
  4. Article
  5. Article
  6. Role ofBiomedicines · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Observational
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.

Rebeca Baz-DávilaResearch Unit, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain.
Adriana Espinoza-JiménezResearch Unit, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain.
María Del Cristo Rodríguez-PérezResearch Unit, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain.
Javier ZuluetaPulmonary Department, Clínica Universitaria de Navarra, Pamplona, Spain.
Nerea VaroBiochemical Analysis Department, Clínica Universitaria de Navarra, Pamplona, Spain.
Ángela MontejoPulmonary Department, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain.
Delia Almeida-GonzálezImmunology Department, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain.
Armando Aguirre-JaimeResearch Unit, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain.
Elizabeth Córdoba-LanúsResearch Unit, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain.
Ciro CasanovaResearch Unit, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain.
Hospital Universitario Nuestra Señora de Candelaria · ESClinica Universidad de Navarra · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia is involved in the development of chronic inflammatory processes. Under hypoxic conditions HIF1A, VEGF and VEGFR2 are expressed and mediate the course of the resultant disease. The aim of the present study was to define the associations between tSNPs in these genes and COPD susceptibility and progression in a Spanish cohort. The T alleles in rs3025020 and rs833070 SNPs (VEGFA gene) were less frequent in the group of COPD cases and were associated with a lower risk of developing the disease (OR = 0.60; 95% CI = 0. 39-0.93; p = 0.023 and OR = 0.60; 95% CI = 0.38-0.96; p = 0.034, respectively) under a dominant model of inheritance. The haplotype in which both SNPs presented the T allele confirmed the association found (OR = 0.02; 95% CI = 0.00 to 0.66; p = 0.03). Moreover, patients with COPD carrying the T allele in homozygosis in rs3025020 SNP showed higher lung function values and this association remained constant during 3 years of follow-up. In conclusion, T allele in rs833070 and rs3025020 may confer a protective effect to COPD susceptibility in a Spanish population and the association of the SNP rs3025020 with lung function may be suggesting a role for VEGF in the progression of the disease.

Indexed as

Polymorphism, Single NucleotideAdultAgedAllelesCase-Control StudiesDisease ProgressionFemaleFollow-Up StudiesGene ExpressionGene FrequencyGenetic Predisposition to DiseaseHaplotypesHomozygoteHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitKDR protein, humanVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2VEGFA protein, human

Identifiers

PMID27163696
PMCPMC4862690
OpenAlexW2439693618

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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.