Evidence map›Paper›PMID 28424691›Full record

ArticleFrontiers in immunology2017

Increased Autophagy-Related 5 Gene Expression Is Associated with Collagen Expression in the Airways of Refractory Asthmatics.

Audrey H Poon, David F Choy, Fazila Chouiali, Rakhee K Ramakrishnan, Bassam Mahboub, Severine Audusseau, Andrea Mogas, Jeffrey M Harris, Joseph R Arron, Catherine Laprise and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.9field-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

33 citing papers in PubMed, 52 citations in OpenAlex.

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  7. Serum autophagy protein 5 is positively related to T helper 2/T helper 1 ratio, inflammation, and exacerbation in adult asthma patients.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2023
    Article
  8. Review
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  16. Autophagy in asthma and chronic obstructive pulmonary disease.Clinical science (London, England : 1979) · 2022
    Article
  17. Article
  18. Article
  19. Article
  20. Autophagy: A Friend or Foe in Allergic Asthma?International journal of molecular sciences · 2021
    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

11 authors at 3 institutions in 2 countries.

Audrey H PoonMeakins-Christie Laboratories, Faculty of Medicine, McGill University, Montreal, QC, Canada.
David F ChoyBiomarker Discovery - OMNI, Genentech Inc., South San Francisco, CA, USA.
Fazila ChouialiMeakins-Christie Laboratories, Faculty of Medicine, McGill University, Montreal, QC, Canada.
Rakhee K RamakrishnanCollege of Medicine, University of Sharjah, Sharjah, United Arab Emirates.
Bassam MahboubCollege of Medicine, University of Sharjah, Sharjah, United Arab Emirates.
Severine AudusseauMeakins-Christie Laboratories, Faculty of Medicine, McGill University, Montreal, QC, Canada.
Andrea MogasMeakins-Christie Laboratories, Faculty of Medicine, McGill University, Montreal, QC, Canada.
Jeffrey M HarrisOMNI Early Clinical Development, Genentech Inc., South San Francisco, CA, USA.
Joseph R ArronImmunology Discovery, Genentech Inc., South San Francisco, CA, USA.
Catherine LapriseMeakins-Christie Laboratories, Faculty of Medicine, McGill University, Montreal, QC, Canada.
Qutayba HamidMeakins-Christie Laboratories, Faculty of Medicine, McGill University, Montreal, QC, Canada.
Christie (Canada) · CAUniversity of Sharjah · AEMcGill University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFibrosis, particularly excessive collagen deposition, presents a challenge for treating asthmatic individuals. At present, no drugs can remove or reduce excessive collagen in asthmatic airways. Hence, the identification of pathways involved in collagen deposition would help to generate therapeutic targets to interfere with the airway remodeling process. Autophagy, a cellular degradation process, has been shown to be dysregulated in various fibrotic diseases, and genetic association studies in independent human populations have identified autophagy-related 5 (ATG5) to be associated with asthma pathogenesis. Hence, the dysregulation of autophagy may contribute to fibrosis in asthmatic airways.

objectiveThis study aimed to determine if (1) collagen deposition in asthmatic airways is associated with ATG5 expression and (2) ATG5 protein expression is associated with asthma

methodsGene expression of transforming growth factor beta 1, various asthma-related collagen types [collagen, type I, alpha 1; collagen, type II, alpha 1; collagen, type III, alpha 1; collagen, type V, alpha 1 (COL5A1) and collagen, type V, alpha 2], and ATG5 were measured using mRNA isolated from bronchial biopsies of refractory asthmatic subjects and assessed for pairwise associations. Protein expression of ATG5 in the airways was measured and associations were assessed for asthma MAIN

resultsIn refractory asthmatic individuals, gene expression of ATG5 was positively associated with COL5A1 in the airways. No association was detected between ATG5 protein expression and asthma CONCLUSION AND CLINICAL RELEVANCE: Positive correlation between the gene expression patterns of ATG5 and COL5A1 suggests that dysregulated autophagy may contribute to subepithelial fibrosis in the airways of refractory asthmatic individuals. This finding highlights the therapeutic potential of ATG5 in ameliorating airway remodeling in the difficult-to-treat refractory asthmatic individuals.

Indexed as

airway remodelingasthmaATG5autophagycollagen

Identifiers

PMID28424691
PMCPMC5372794
OpenAlexW2603793890

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.