Evidence map›Paper›PMID 27562142›Full record

ArticleScientific reports2016

Thromboxane A2 exacerbates acute lung injury via promoting edema formation.

Koji Kobayashi, Daiki Horikami, Keisuke Omori, Tatsuro Nakamura, Arisa Yamazaki, Shingo Maeda, Takahisa Murata

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Review
  7. Article
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  16. Review
  17. Article
  18. Review
  19. Article
  20. American journal of physiology. Heart and circulatory physiology · 2021
    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

7 authors at 1 institution in 1 country.

Koji KobayashiDepartment of Animal Radiology, Graduate school of Agriculture and Life Sciences, The University of Tokyo, Japan.
Daiki HorikamiDepartment of Animal Radiology, Graduate school of Agriculture and Life Sciences, The University of Tokyo, Japan.
Keisuke OmoriDepartment of Animal Radiology, Graduate school of Agriculture and Life Sciences, The University of Tokyo, Japan.
Tatsuro NakamuraDepartment of Animal Radiology, Graduate school of Agriculture and Life Sciences, The University of Tokyo, Japan.
Arisa YamazakiDepartment of Animal Radiology, Graduate school of Agriculture and Life Sciences, The University of Tokyo, Japan.
Shingo MaedaDepartment of Animal Radiology, Graduate school of Agriculture and Life Sciences, The University of Tokyo, Japan.
Takahisa MurataDepartment of Animal Radiology, Graduate school of Agriculture and Life Sciences, The University of Tokyo, Japan.
The University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thromboxane A2 (TXA2) is produced in the lungs of patients suffering from acute lung injury (ALI). We assessed its contribution in disease progression using three different ALI mouse models. The administration of hydrochloric acid (HCl) or oleic acid (OA)+ lipopolysaccharide (LPS) caused tissue edema and neutrophil infiltration with TXA2 production in the lungs of the experimental mice. The administration of LPS induced only neutrophil accumulation without TXA2 production. Pretreatment with T prostanoid receptor (TP) antagonist attenuated the tissue edema but not neutrophil infiltration in these models. Intravital imaging and immunostaining demonstrated that administration of TP agonist caused vascular hyper-permeability by disrupting the endothelial barrier formation in the mouse ear. In vitro experiments showed that TP-stimulation disrupted the endothelial adherens junction, and it was inhibited by Ca(2+) channel blockade or Rho kinase inhibition. Thus endogenous TXA2 exacerbates ALI, and its blockade attenuates it by modulating the extent of lung edema. This can be explained by the endothelial hyper-permeability caused by the activation of TXA2-TP axis, via Ca(2+)- and Rho kinase-dependent signaling.

Indexed as

Acute Lung InjuryAnimalsHydrochloric AcidLipopolysaccharidesMaleMiceMice, Inbred BALB CNeutrophil InfiltrationNeutrophilsOleic AcidPulmonary EdemaThromboxane A2Hydrochloric AcidLipopolysaccharidesOleic AcidThromboxane A2

Identifiers

PMID27562142
PMCPMC4999811
OpenAlexW2513997196

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.