Evidence map›Paper›PMID 28522564›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2017

Decreased phosphatase PTEN amplifies PI3K signaling and enhances proinflammatory cytokine release in COPD.

Satoru Yanagisawa, Jonathan R Baker, Chaitanya Vuppusetty, Peter Fenwick, Louise E Donnelly, Kazuhiro Ito, Peter J Barnes

Open access · hybridAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.1field-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

31 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
  2. Article
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  6. Senotherapy for chronic lung disease.Pharmacological reviews · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Unveiling mechanisms of lung aging in COPD: A promising target for therapeutics development.Chinese medical journal pulmonary and critical care medicine · 2024
    Review
  11. A miRNA-21-Mediated PTEN/Akt/NF-κB Axis Promotes Chronic Obstructive Pulmonary Disease Pathogenesis.International journal of chronic obstructive pulmonary disease · 2024
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Long noncoding RNAActa biochimica et biophysica Sinica · 2022
    Article
  17. Review
  18. Article
  19. Review
  20. 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

7 authors at 1 institution in 1 country.

Satoru YanagisawaAirway Disease Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Jonathan R BakerAirway Disease Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Chaitanya VuppusettyAirway Disease Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Peter FenwickAirway Disease Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Louise E DonnellyAirway Disease Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Kazuhiro ItoAirway Disease Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Peter J BarnesAirway Disease Section, National Heart and Lung Institute, Imperial College London, London, United Kingdom p.j.barnes@imperial.ac.uk.
Imperial College London · GB

Funding

Wellcome Trust 093080/Z/10/Z
6 · The paper itself

Abstract

The phosphatidylinositol 3-kinase (PI3K) pathway is activated in chronic obstructive pulmonary disease (COPD), but the regulatory mechanisms for this pathway are yet to be elucidated. The aim of this study was to determine the expression and role of phosphatase and tensin homolog deleted from chromosome 10 (PTEN), a negative regulator of the PI3K pathway, in COPD. PTEN protein expression was measured in the peripheral lung of COPD patients compared with smoking and nonsmoking controls. The direct influence of cigarette smoke extract (CSE) on PTEN expression was assessed using primary lung epithelial cells and a cell line (BEAS-2B) in the presence or absence of l-buthionine-sulfoximine (BSO) to deplete intracellular glutathione. The impact of PTEN knockdown by RNA interference on cytokine production was also examined. In peripheral lung, PTEN protein was significantly decreased in patients with COPD compared with the subjects without COPD (

Indexed as

AgedCell LineCytokinesEpithelial CellsFemaleHumansInflammationLungMaleOxidative StressPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePulmonary Disease, Chronic ObstructiveSignal TransductionCytokinesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanSmokechronic obstructive pulmonary diseaseoxidative stressphosphatase and tensin homolog deleted from chromosome 10PI3K IL-6

Identifiers

PMID28522564
PMCPMC5582930
OpenAlexW2615942550

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.