Evidence map›Paper›PMID 27189668›Full record

ReviewNature reviews. Disease primers2015

Asthma.

Stephen T Holgate, Sally Wenzel, Dirkje S Postma, Scott T Weiss, Harald Renz, Peter D Sly

Open access · bronzeAbstract readReview
In one paragraph

Review in Nature reviews. Disease primers, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 374 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
374citing papers in PubMed, 4 pooled it
9.4field-weighted citation impact, top 1% 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

374 citing papers in PubMed, 4 syntheses or guidelines pooled it, 621 citations in OpenAlex.

  1. Pooled it
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  9. Biologic effectiveness increases with earlier biologic initiation after severe asthma onset.The journal of allergy and clinical immunology. Global · 2026
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  20. The causal relationships between childhood-onset asthma and major mental disorders: an MR study.European archives of psychiatry and clinical neuroscience · 2026
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314 more citing papers are in PubMed but not listed here.

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 5 institutions in 4 countries.

Stephen T HolgateClinical and Experimental Sciences, Mail Point 810, Level F, Sir Henry Wellcome Building, Southampton General Hospital, Southampton, SO16 6YD, UK.
Sally WenzelSubsection Chief of Allergy, Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh, Asthma Institute at UPMC/UPSOM, Pittsburgh, Pennsylvania, USA.
Dirkje S PostmaUniversity of Groningen, University Medical Center Groningen, Department of Pulmonology, Groningen, the Netherlands.
Scott T WeissChanning Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Harald RenzInstitute of Laboratory Medicine and Pathobiochemistry, Molecular Diagnostics, Philipps University Marburg, University Hospital Giessen and Marburg GmbH, Campus Marburg, Marburg, Germany.
Peter D SlyQueensland Children's Medical Research Institute and Centre for Child Health Research, University of Queensland, Brisbane, Australia.
Brigham and Women's Hospital · USQueensland Children’s Medical Research Institute · AUUniversitätsklinikum Gießen und Marburg · DEUniversity Medical Center Groningen · NLUniversity of Pittsburgh · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma is the most common inflammatory disease of the lungs. The prevalence of asthma is increasing in many parts of the world that have adopted aspects of the Western lifestyle, and the disease poses a substantial global health and economic burden. Asthma involves both the large-conducting and the small-conducting airways, and is characterized by a combination of inflammation and structural remodelling that might begin in utero. Disease progression occurs in the context of a developmental background in which the postnatal acquisition of asthma is strongly linked with allergic sensitization. Most asthma cases follow a variable course, involving viral-induced wheezing and allergen sensitization, that is associated with various underlying mechanisms (or endotypes) that can differ between individuals. Each set of endotypes, in turn, produces specific asthma characteristics that evolve across the lifecourse of the patient. Strong genetic and environmental drivers of asthma interconnect through novel epigenetic mechanisms that operate prenatally and throughout childhood. Asthma can spontaneously remit or begin de novo in adulthood, and the factors that lead to the emergence and regression of asthma, irrespective of age, are poorly understood. Nonetheless, there is mounting evidence that supports a primary role for structural changes in the airways with asthma acquisition, on which altered innate immune mechanisms and microbiota interactions are superimposed. On the basis of the identification of new causative pathways, the subphenotyping of asthma across the lifecourse of patients is paving the way for more-personalized and precise pathway-specific approaches for the prevention and treatment of asthma, creating the real possibility of total prevention and cure for this chronic inflammatory disease.

Indexed as

AsthmaAllergensDisease ProgressionEpigenesis, GeneticHumansHypersensitivityPhenotypeRespiratory SoundsAllergens

Identifiers

PMID27189668
PMCPMC7096989
OpenAlexW4210991698

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.