Evidence map›Paper›PMID 26069107›Full record

ReviewYonsei medical journal2015

Gene-Environment Interactions in Asthma: Genetic and Epigenetic Effects.

Jong-Uk Lee, Jeong Dong Kim, Choon-Sik Park

Open access · goldAbstract readReview
In one paragraph

Review in Yonsei medical journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 55 citations in OpenAlex.

  1. Trial
  2. Mechanisms and therapeutic strategies of asthma: from bench to bedside.Signal transduction and targeted therapy · 2026
    Review
  3. Article
  4. Current understanding and future directions in severe asthma through artificial intelligence-integrated multi-omic approaches.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  5. Article
  6. Article
  7. Bacteria and Allergic Diseases.International journal of molecular sciences · 2024
    Review
  8. Review
  9. Effect of Src tyrosine kinase on a rat model of asthma.Experimental and therapeutic medicine · 2022
    Article
  10. Review
  11. The risk of atopic dermatitis may be affected byPostepy dermatologii i alergologii · 2021
    Article
  12. Second-hand smoke and NFE2L2 genotype interaction increases paediatric asthma risk and severity.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2021
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Immunological Factors Associated with Adult Asthma in the Aseer Region, Southwestern Saudi Arabia.International journal of environmental research and public health · 2019
    Article
  20. 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

3 authors at 2 institutions in 1 country.

Jong-Uk LeeDepartment of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang Graduate School, Bucheon, Korea.
Jeong Dong KimDepartment of Interdisciplinary Program in Biomedical Science Major, Soonchunhyang Graduate School, Bucheon, Korea.
Choon-Sik ParkGenome Research Center and Division of Allergy and Respiratory Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Korea. mdcspark@daum.net.
Soonchunhyang University · KRBucheon University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the past three decades, a large number of genetic studies have been aimed at finding genetic variants associated with the risk of asthma, applying various genetic and genomic approaches including linkage analysis, candidate gene polymorphism studies, and genome-wide association studies (GWAS). However, contrary to general expectation, even single nucleotide polymorphisms (SNPs) discovered by GWAS failed to fully explain the heritability of asthma. Thus, application of rare allele polymorphisms in well defined phenotypes and clarification of environmental factors have been suggested to overcome the problem of 'missing' heritability. Such factors include allergens, cigarette smoke, air pollutants, and infectious agents during pre- and post-natal periods. The first and simplest interaction between a gene and the environment is a candidate interaction of both a well known gene and environmental factor in a direct physical or chemical interaction such as between CD14 and endotoxin or between HLA and allergens. Several GWAS have found environmental interactions with occupational asthma, aspirin exacerbated respiratory disease, tobacco smoke-related airway dysfunction, and farm-related atopic diseases. As one of the mechanisms behind gene-environment interaction is epigenetics, a few studies on DNA CpG methylation have been reported on subphenotypes of asthma, pitching the exciting idea that it may be possible to intervene at the junction between the genome and the environment. Epigenetic studies are starting to include data from clinical samples, which will make them another powerful tool for re-search on gene-environment interactions in asthma.

Indexed as

Epigenesis, GeneticGene-Environment InteractionPolymorphism, GeneticAllelesAllergensAsthmaEndotoxinsEnvironmentGenome-Wide Association StudyHumansPhenotypePolymorphism, Single NucleotideAllergensEndotoxinsAsthmaenvironmentepigeneticsgenegenomepolymorphismvariants

Identifiers

PMID26069107
PMCPMC4479853
OpenAlexW1704575732

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.