Evidence map›Paper›PMID 25478196›Full record

ReviewJournal of thoracic disease2014

Targeting pro-resolution pathways to combat chronic inflammation in COPD.

Steven Bozinovski, Desiree Anthony, Ross Vlahos

Open access · greenAbstract readReview
In one paragraph

Review in Journal of thoracic disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 39 citations in OpenAlex.

  1. Observational
  2. Article
  3. Review
  4. Article
  5. Pathophysiological Role of Vimentin Intermediate Filaments in Lung Diseases.Frontiers in cell and developmental biology · 2022
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Annexin A1 is elevated in patients with COPD and affects lung fibroblast function.International journal of chronic obstructive pulmonary disease · 2018
    Article
  11. Article
  12. Review
  13. Review
  14. Observational
  15. Review
  16. Resolvin D1 Reduces Emphysema and Chronic Inflammation.The American journal of pathology · 2015
    Article
  17. Article
  18. 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.

Steven BozinovskiLung Health Research Centre, Department of Pharmacology and Therapeutics, The University of Melbourne, Parkville 3010, Australia.
Desiree AnthonyLung Health Research Centre, Department of Pharmacology and Therapeutics, The University of Melbourne, Parkville 3010, Australia.
Ross VlahosLung Health Research Centre, Department of Pharmacology and Therapeutics, The University of Melbourne, Parkville 3010, Australia.
The University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is an inflammatory lung condition that is associated with irreversible airflow obstruction as a consequence of small airways disease, excessive mucus production and emphysema. Paradoxically, excessive inflammation fails to control microbial pathogens that not only colonise COPD airways, but also trigger acute exacerbations, which markedly increase inflammation underlying host tissue damage. Excessive production of leukocyte mobilising cytokines such as CXCL8 (IL-8) and leukotriene B4 (LTB4) in response to environmental stimuli (cigarette smoke and microbial products) are thought to maintain chronic inflammation, in conjunction with inefficient macrophage clearance of microbes and apoptotic neutrophils. In this perspective, we discuss an alternative view on why inflammation persists with a focus on why pro-resolution mediators such as lipoxin A4 (LXA4), D-series resolving and Annexin A1 fail to effectively switch off inflammation in COPD. These pro-resolving mediators converge on the G-protein coupled receptor, ALX/FPR2. This receptor is particularly relevant to COPD as the complex milieu of exogenous and host-derived mediators within the inflamed airways include agonists that potently activate ALX/FPR2, including Serum Amyloid A (SAA) and the cathelicidin, LL-37. There is emerging evidence to suggest that ALX/FPR2 can exist in alternative receptor conformations in an agonist-biased manner, which facilitates alternate functional receptor behaviors. Hence, the development of more stable pro-resolving analogs provides therapeutic opportunities to address ALX/FPR2 conformations to counteract pathogenic signaling and promote non-phlogistic clearance pathways essential for resolution of inflammation.

Indexed as

ALX/FPR2catabasischronic obstructive pulmonary disease (COPD)inflammationresolutionSerum Amyloid A (SAA)

Identifiers

PMID25478196
PMCPMC4255161
OpenAlexW2106914617

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.