Evidence map›Paper›PMID 33778909›Full record

ArticleIntensive care medicine experimental2021

A role for bronchial epithelial autotaxin in ventilator-induced lung injury.

Ioanna Nikitopoulou, Ioanna Ninou, Nikolaos Manitsopoulos, Ioanna Dimopoulou, Stylianos E Orfanos, Vassilis Aidinis, Anastasia Kotanidou

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Intensive care medicine experimental, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 42% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. [Value of autotaxin in predicting refractoryZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2022
    Article
  7. 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 3 institutions in 1 country.

Ioanna Nikitopoulou1st Department of Critical Care Medicine & Pulmonary Services, GP Livanos and M Simou Laboratories, National and Kapodistrian University of Athens Medical School, Evangelismos Hospital, 45, Ipsilantou Street, Athens, Greece.
Ioanna NinouInstitute of Immunology, Biomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Nikolaos Manitsopoulos1st Department of Critical Care Medicine & Pulmonary Services, GP Livanos and M Simou Laboratories, National and Kapodistrian University of Athens Medical School, Evangelismos Hospital, 45, Ipsilantou Street, Athens, Greece.
Ioanna Dimopoulou1st Department of Critical Care Medicine & Pulmonary Services, National and Kapodistrian University of Athens Medical School, Evangelismos Hospital, 45, Ipsilantou Street, Athens, Greece.
Stylianos E Orfanos1st Department of Critical Care Medicine & Pulmonary Services, GP Livanos and M Simou Laboratories, National and Kapodistrian University of Athens Medical School, Evangelismos Hospital, 45, Ipsilantou Street, Athens, Greece.
Vassilis AidinisInstitute of Immunology, Biomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Anastasia Kotanidou1st Department of Critical Care Medicine & Pulmonary Services, GP Livanos and M Simou Laboratories, National and Kapodistrian University of Athens Medical School, Evangelismos Hospital, 45, Ipsilantou Street, Athens, Greece. akotanid@med.uoa.gr.
National and Kapodistrian University of Athens · GRAlexander Fleming Biomedical Sciences Research Center · GREvangelismos Hospital · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe pathophysiology of acute respiratory distress syndrome (ARDS) may eventually result in heterogeneous lung collapse and edema-flooded airways, predisposing the lung to progressive tissue damage known as ventilator-induced lung injury (VILI). Autotaxin (ATX; ENPP2), the enzyme largely responsible for extracellular lysophosphatidic acid (LPA) production, has been suggested to play a pathogenic role in, among others, pulmonary inflammation and fibrosis.

methodsC57BL/6 mice were subjected to low and high tidal volume mechanical ventilation using a small animal ventilator: respiratory mechanics were evaluated, and plasma and bronchoalveolar lavage fluid (BALF) samples were obtained. Total protein concentration was determined, and lung histopathology was further performed

resultsInjurious ventilation resulted in increased BALF levels of ATX. Genetic deletion of ATX from bronchial epithelial cells attenuated VILI-induced pulmonary edema.

conclusionATX participates in VILI pathogenesis.

Indexed as

AutotaxinEdemaLung functionMechanical ventilation

Identifiers

PMID33778909
PMCPMC8005331
OpenAlexW3150941303

What Socratic 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 Socratic graph.