Evidence map›Paper›PMID 28547381›Full record

ReviewPurinergic signalling2017

Purinergic signalling links mechanical breath profile and alveolar mechanics with the pro-inflammatory innate immune response causing ventilation-induced lung injury.

Djo Hasan, Paul Blankman, Gary F Nieman

Open access · hybridAbstract readReview
In one paragraph

Review in Purinergic signalling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  7. Article
  8. Review
  9. Hyperoxia and modulation of pulmonary vascular and immune responses in COVID-19.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  10. Damage-associated molecular patterns in trauma.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2020
    Review
  11. P2 Purinergic Signaling in the Distal Lung in Health and Disease.International journal of molecular sciences · 2020
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Observational
  18. Recent advances in CD8Oncology letters · 2018
    Review
  19. Danger signals from mitochondrial DAMPS in trauma and post-injury sepsis.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2018
    Review
  20. Acute lung injury: how to stabilize a broken lung.Critical care (London, England) · 2018
    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 2 institutions in 2 countries.

Djo HasanDepartment of Adult ICU, University Hospital Erasmus MC Rotterdam, 's-Gravendijkwal 230 3015 CE, Rotterdam, the Netherlands. djohasan@gmail.com.ORCID 0000-0003-4610-5433
Paul BlankmanDepartment of Adult ICU, University Hospital Erasmus MC Rotterdam, 's-Gravendijkwal 230 3015 CE, Rotterdam, the Netherlands.
Gary F NiemanDepartment of Surgery, Upstate Medical University, 750 E Adams St, Syracuse, NY, 13210, USA.
Erasmus MC · NLSUNY Upstate Medical University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe pulmonary infection or vigorous cyclic deformation of the alveolar epithelial type I (AT I) cells by mechanical ventilation leads to massive extracellular ATP release. High levels of extracellular ATP saturate the ATP hydrolysis enzymes CD39 and CD73 resulting in persistent high ATP levels despite the conversion to adenosine. Above a certain level, extracellular ATP molecules act as danger-associated molecular patterns (DAMPs) and activate the pro-inflammatory response of the innate immunity through purinergic receptors on the surface of the immune cells. This results in lung tissue inflammation, capillary leakage, interstitial and alveolar oedema and lung injury reducing the production of surfactant by the damaged AT II cells and deactivating the surfactant function by the concomitant extravasated serum proteins through capillary leakage followed by a substantial increase in alveolar surface tension and alveolar collapse. The resulting inhomogeneous ventilation of the lungs is an important mechanism in the development of ventilation-induced lung injury. The high levels of extracellular ATP and the upregulation of ecto-enzymes and soluble enzymes that hydrolyse ATP to adenosine (CD39 and CD73) increase the extracellular adenosine levels that inhibit the innate and adaptive immune responses rendering the host susceptible to infection by invading microorganisms. Moreover, high levels of extracellular adenosine increase the expression, the production and the activation of pro-fibrotic proteins (such as TGF-β, α-SMA, etc.) followed by the establishment of lung fibrosis.

Indexed as

AdenosineAnimalsHumansImmunity, InnateInflammationLung InjuryPurinergic AgentsReceptors, PurinergicAdenosinePurinergic AgentsReceptors, PurinergicCD39CD73Diffuse alveolar damageExtracellular ATPPurinergic signallingVentilation-induced lung injury

Identifiers

PMID28547381
PMCPMC5563293
OpenAlexW2619776216

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.