Evidence map›Paper›PMID 26335713›Full record

ReviewAllergy2016

Autophagy in airway diseases: a new frontier in human asthma?

A A Zeki, B Yeganeh, N J Kenyon, M Post, S Ghavami

Open access · bronzeAbstract readReview
In one paragraph

Review in Allergy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Article
  3. Association of genetic variants in the autophagy gene ATG4B with asthma.medRxiv : the preprint server for health sciences · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Evaluation of Autophagy in Conjunctival Fibroblasts.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  8. Blockage of Autophagy for Cancer Therapy: A Comprehensive Review.International journal of molecular sciences · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Role of autophagy in lung diseases and ageing.European respiratory review : an official journal of the European Respiratory Society · 2022
    Review
  16. Review
  17. Article
  18. Review
  19. Article
  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

5 authors at 4 institutions in 2 countries.

A A ZekiDivision of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Center for Comparative Respiratory Biology and Medicine, Davis, CA, USA.
B YeganehPhysiology and Experimental Medicine, Hospital for Sick Children (Sickkids), University of Toronto, Toronto, ON, Canada.
N J KenyonDivision of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, Center for Comparative Respiratory Biology and Medicine, Davis, CA, USA.
M PostPhysiology and Experimental Medicine, Hospital for Sick Children (Sickkids), University of Toronto, Toronto, ON, Canada.
S GhavamiDepartment of Human Anatomy & Cell Science, Faculty of Health Sciences, College of Medicine, University of Manitoba, Winnipeg, MB, Canada.
University of California, Davis · USSickKids Foundation · CAUniversity of Manitoba · CAUniversity of Toronto · CA

Funding

The Modulation of Eotaxin Expression by Statins: Implications for Asthma TherapyK08HL114882 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI ZEKI, AMIR A. · 2014 to 2016
$435k
NHLBI NIH HHS 1K08HL114882-01A1NHLBI NIH HHS K08 HL114882NHLBI NIH HHS L30 HL104807
6 · The paper itself

Abstract

The study of autophagy ('self-eating'), a fundamental cell fate pathway involved in physiological and pathological subcellular processes, opens a new frontier in the continuous search for novel therapies for human asthma. Asthma is a complex syndrome with different disease phenotypes. Autophagy plays a central role in cell physiology, energy and metabolism, and cell survival. Autophagy's hallmark is the formation of double-membrane autophagic autophagosomes, and this process is operational in airway epithelial and mesenchymal cells in asthma. Genetic associations between autophagy genes and asthma have been observed including single nucleotide polymorphisms in Atg5 which correlate with reduced lung function. Immune mechanisms important in asthma such as Th2 cells and eosinophils also manifest autophagy. Lastly, we address the role of autophagy in extracellular matrix deposition and fibrosis in asthmatic airways remodeling, a pathologic process still without effective therapy, and discuss potential pharmacologic inhibitors. We end by offering two opposing but plausible hypotheses as to how autophagy may be directly involved in airway fibrosis.

Indexed as

AutophagyAirway RemodelingAnimalsAnti-Asthmatic AgentsAsthmaDisease Models, AnimalExtracellular MatrixFibrosisGenetic Predisposition to DiseaseHumansImmunityAnti-Asthmatic Agentsasthmaautophagyfibrosishypothesesremodeling

Identifiers

PMID26335713
PMCPMC4715640
OpenAlexW1894136033

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.