Evidence map›Paper›PMID 23536202›Full record

ReviewSeminars in immunopathology2013

The UPR and lung disease.

Fabiola Osorio, Bart Lambrecht, Sophie Janssens

Abstract readReview
PubMed Publisher
In one paragraph

Review in Seminars in immunopathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

39 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Review
  3. Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025
    Review
  4. Article
  5. Understanding the impact of ER stress on lung physiology.Frontiers in cell and developmental biology · 2024
    Review
  6. Article
  7. Endoplasmic reticulum stress: a vital process and potential therapeutic target in chronic obstructive pulmonary disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. The HMGB1-RAGE axis induces apoptosis in acute respiratory distress syndrome through PERK/eIF2α/ATF4-mediated endoplasmic reticulum stress.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  12. Article
  13. Mechanisms Targeting the Unfolded Protein Response in Asthma.American journal of respiratory cell and molecular biology · 2021
    Review
  14. Article
  15. Review
  16. Aging and Lung Disease.Annual review of physiology · 2020
    Review
  17. Review
  18. The Role of Heat Shock Protein 70 kDa in Asthma.Journal of asthma and allergy · 2020
    Review
  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 1 institution in 1 country.

Fabiola OsorioGROUP-ID Consortium, Laboratory of Immunoregulation and Mucosal Immunology, Department of Respiratory Diseases, University Hospital, Ghent, Belgium.
Bart Lambrecht
Sophie Janssens
Ghent University Hospital · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The respiratory tract has a surface area of approximately 70 m(2) that is in direct contact with the external environment. Approximately 12,000 l of air are inhaled daily, exposing the airway epithelium to up to 25 million particles an hour. Several inhaled environmental triggers, like cigarette smoke, diesel exhaust, or allergens, are known inducers of endoplasmatic reticulum (ER) stress and cause a dysregulation in ER homeostasis. Furthermore, some epithelial cell types along the respiratory tract have a secretory function, producing large amounts of mucus or pulmonary surfactant, as well as innate host defense molecules like defensins. To keep up with their secretory demands, these cells must rely on the appropriate functioning and folding capacity of the ER, and they are particularly more vulnerable to conditions of unresolved ER stress. In the lung interstitium, triggering of ER stress pathways has a major impact on the functioning of vascular smooth muscle cells and fibroblasts, causing aberrant dedifferentiation and proliferation. Given the large amounts of foreign material inhaled, the lung is densely populated by various types of immune cells specialized in engulfing and killing pathogens and in secreting cytokines/chemokines for efficient microbial clearance. Unfolded protein response signaling cascades have been shown to intersect with the functioning of immune cells at all levels. The current review aims to highlight the role of ER stress in health and disease in the lung, focusing on its impact on different structural and inflammatory cell types.

Indexed as

Unfolded Protein ResponseAnimalsEndoplasmic Reticulum StressEnvironmentHumansLungLung Diseases

Identifiers

PMID23536202
OpenAlexW2089886478

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.