Evidence map›Paper›PMID 27561663›Full record

ReviewClinical reviews in allergy & immunology2019

CD26 and Asthma: a Comprehensive Review.

Juan J Nieto-Fontarigo, Francisco J González-Barcala, Esther San José, Pilar Arias, Montserrat Nogueira, Francisco J Salgado

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical reviews in allergy & immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
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  14. Association between Dipeptidyl Peptidase-4 Inhibitors and Allergic Rhinitis in Asian Patients with Diabetes.International journal of environmental research and public health · 2019
    Article
  15. Article
  16. Diabetes and Lung Disease: A Neglected Relationship.The review of diabetic studies : RDS · 2019
    Review
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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

6 authors at 2 institutions in 1 country.

Juan J Nieto-FontarigoDepartment of Biochemistry and Molecular Biology, Faculty of Biology-Biological Research Centre (CIBUS), University of Santiago de Compostela (USC), Santiago de Compostela, Spain.
Francisco J González-BarcalaDepartment of Biochemistry and Molecular Biology, Faculty of Biology-Biological Research Centre (CIBUS), University of Santiago de Compostela (USC), Santiago de Compostela, Spain.
Esther San JoséClinical Analysis Service, Clinic University Hospital (CHUS), Santiago de Compostela, Spain.
Pilar AriasDepartment of Biochemistry and Molecular Biology, Faculty of Biology-Biological Research Centre (CIBUS), University of Santiago de Compostela (USC), Santiago de Compostela, Spain.
Montserrat NogueiraDepartment of Biochemistry and Molecular Biology, Faculty of Biology-Biological Research Centre (CIBUS), University of Santiago de Compostela (USC), Santiago de Compostela, Spain.
Francisco J SalgadoDepartment of Biochemistry and Molecular Biology, Faculty of Biology-Biological Research Centre (CIBUS), University of Santiago de Compostela (USC), Santiago de Compostela, Spain. franciscojavier.salgado@usc.es.
Universidade de Santiago de Compostela · ESComplejo Hospitalario Universitario de Santiago · ES

Funding

Instituto de Salud Carlos III PI13/02046Sociedad Española de Neumología y Cirugía Torácica 121/2012
6 · The paper itself

Abstract

Asthma is a heterogeneous and chronic inflammatory family of disorders of the airways with increasing prevalence that results in recurrent and reversible bronchial obstruction and expiratory airflow limitation. These diseases arise from the interaction between environmental and genetic factors, which collaborate to cause increased susceptibility and severity. Many asthma susceptibility genes are linked to the immune system or encode enzymes like metalloproteases (e.g., ADAM-33) or serine proteases. The S9 family of serine proteases (prolyl oligopeptidases) is capable to process peptide bonds adjacent to proline, a kind of cleavage-resistant peptide bonds present in many growth factors, chemokines or cytokines that are important for asthma. Curiously, two serine proteases within the S9 family encoded by genes located on chromosome 2 appear to have a role in asthma: CD26/dipeptidyl peptidase 4 (DPP4) and DPP10. The aim of this review is to summarize the current knowledge about CD26 and to provide a structured overview of the numerous functions and implications that this versatile enzyme could have in this disease, especially after the detection of some secondary effects (e.g., viral nasopharyngitis) in type II diabetes mellitus patients (a subset with a certain risk of developing obesity-related asthma) upon CD26 inhibitory therapy.

Indexed as

AnimalsAsthmaBiomarkersBody FluidsCD4-Positive T-LymphocytesChemokinesCytokinesDipeptidyl Peptidase 4Disease Models, AnimalGenetic Predisposition to DiseaseHumansMultigene FamilyPhenotypeProlyl OligopeptidasesSerine EndopeptidasesSeverity of Illness IndexBiomarkersChemokinesCytokinesDipeptidyl Peptidase 4PREPL protein, humanProlyl OligopeptidasesSerine EndopeptidasesAsthmaCD26CD26 inhibitorsCytokines and chemokinesDPP4sCD26

Identifiers

PMID27561663
PMCPMC7090975
OpenAlexW2518282857

What OpenQuestion holds

Textmetadata
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.