Evidence map›Paper›PMID 24817794›Full record

ReviewMediators of inflammation2014

ADAM metallopeptidase domain 33 (ADAM33): a promising target for asthma.

Priya Tripathi, Shally Awasthi, Peisong Gao

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
2.6field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. 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
  3. Article
  4. Review
  5. Article
  6. ADAM33's Role in Asthma Pathogenesis: An Overview.International journal of molecular sciences · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Interactions via αInternational journal of molecular sciences · 2021
    Article
  14. The Association of IgE Levels withJournal of personalized medicine · 2021
    Article
  15. Airway hyperresponsiveness development and the toxicity of PM2.5.Environmental science and pollution research international · 2021
    Review
  16. Epigenetic Changes in Asthma: Role of DNA CpG Methylation.Tuberculosis and respiratory diseases · 2020
    Review
  17. Haplotype analysis ofThe Indian journal of medical research · 2019
    Article
  18. Article
  19. Review
  20. Article
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 2 countries.

Priya TripathiJohns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine, 5501 Hopkins Bayview Circle, Room 3B.71, Baltimore, MD 21224, USA.
Shally AwasthiDepartment of Pediatrics, King George's Medical University, Lucknow, India.
Peisong GaoJohns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine, 5501 Hopkins Bayview Circle, Room 3B.71, Baltimore, MD 21224, USA.
Johns Hopkins University · USKing George's Medical University · IN

Funding

Sensitization to Cockroach Allergen: Immune Regulation and Genetic DeterminantsR01ES021739 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI GAO, PEISONG · 2013 to 2017
$1.8M
NIEHS NIH HHS R01 ES021739NIEHS NIH HHS R01ES021739-01A1
6 · The paper itself

Abstract

Over the last few years, a significant progress has been made in understanding the role of a disintegrin and metalloproteinase 33 (ADAM33) in asthma. The previous observations for the association with asthma have been replicated in over 33 different population samples worldwide. We and others have performed association analysis and meta-analysis and provided further evidence that several polymorphisms in the ADAM33 are risk factors for asthma, especially in the Asian population. Further, several studies have suggested that alterations in epigenetic marks alter the patterns of DNA methylation of ADAM33 and result in potentially adverse biological effects. Finally, while the biological activities of ADAM33 are as yet unknown, ADAM33 may play a possible role in airway remodeling because of its high expression in epithelium, myo/fibroblasts, and airway smooth muscle cells (ASMCs) and its role in promoting angiogenesis and stimulating cell proliferation and differentiation. Thus, ADAM33 represents a promising target for asthma. However, further investigations are clearly needed to discover functional ADAM33 gene polymorphisms and the role of genetic/epigenetic factors in conferring genetic susceptibility to environmental exposure induced asthma as well as biological function in asthma. This, in turn, will unlock the possibility of ADAM33 as a target for asthma therapy.

Indexed as

ADAM ProteinsAirway RemodelingAnimalsAsthmaHumansMyocytes, Smooth MusclePolymorphism, GeneticADAM33 protein, humanADAM Proteins

Identifiers

PMID24817794
PMCPMC4003756
OpenAlexW1981245898

What OpenQuestion holds

Textmetadata
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.