Evidence map›Paper›PMID 19226616›Full record

ArticleAnatomical record (Hoboken, N.J. : 2007)2009

Role of protease activated receptor 2 in experimental acute lung injury and lung fibrosis.

Xiao Su, Michael A Matthay

Open access · greenAbstract read
In one paragraph

Article in Anatomical record (Hoboken, N.J. : 2007), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  4. Protease-activated receptor 1 as a potential therapeutic target for COVID-19.Experimental biology and medicine (Maywood, N.J.) · 2021
    Review
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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

2 authors at 1 institution in 1 country.

Xiao SuCardiovascular Research Institute, University of California, San Francisco, CA 94143-0130, USA. suxiao1@yahoo.com
Michael A Matthay
University of California, San Francisco · US

Funding

MECHANISMS OF ALVEOLAR EPITHELIAL FLUID CLEARANCER01HL051854 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MATTHAY, MICHAEL A. · 1994 to 2012
$4.4M
Resolution of Clinical Lung InjuryR37HL051856 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MATTHAY, MICHAEL A. · 2006 to 2015
$3.9M
RESOLUTION OF CLINICAL LUNG INJURYR01HL051856 · NHLBI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI MATTHAY, MICHAEL A. · 1996 to 2005
$1.7M
High-performance Food Pathogen Detection InstrumentR44RR018420 · NCRR · BIODETECTION INSTRUMENTS, LLC · PI SU, XIAOLI · 2005 to 2006
$755k
NCRR NIH HHS R44 RR018420NHLBI NIH HHS HL-51854NHLBI NIH HHS HL-51856NHLBI NIH HHS R01 HL051854NHLBI NIH HHS R01 HL051856NHLBI NIH HHS R37 HL051856
6 · The paper itself

Abstract

Protease activated receptor 2 (PAR2) is widely-distributed (lung, liver, kidney, etc.) and expressed by variety of cells (i.e. leukocytes, epithelial cells, endothelial cells, and fibroblast). PAR2 may participate in many pathological processes, such as, inflammation, injury, as well as fibrosis. Therefore, in this study, we tested whether PAR2 would exert a role in acid-induced acute lung injury, E. coli pneumonia, bleomycin-induced acute lung injury and fibrosis. Acid, E. coli, or bleomycin were intratracheally instilled into the lungs of both wildtype and PAR2 knockout mice to detect differences in pulmonary edema, lung vascular permeability, lung fibrosis, and other parameters. Knockout of PAR2 did not affect the extent of pulmonary edema and lung vascular permeability in acid-induced acute lung injury. Also, both activation of PAR2 in the airspaces of the lung and deletion of PAR2 did not alter the magnitude of pulmonary edema and lung vascular permeability in E. coli pneumonia. Finally, PAR2 deficiency did not affect the severity of lung inflammation and lung fibrosis in bleomycin-induced acute lung injury and lung fibrosis models. Thus, PAR2 does not appear to play a critical role in the pathogeneses of experimental acid-induced acute lung injury, E. coli pneumonia, and bleomycin-induced acute lung injury and pulmonary fibrosis in mice.

Indexed as

Acute Lung InjuryAnimalsAntibiotics, AntineoplasticBleomycinCapillariesCapillary PermeabilityDisease Models, AnimalEscherichia coli InfectionsLungMiceMice, KnockoutPneumonia, BacterialPulmonary AlveoliPulmonary EdemaPulmonary FibrosisReceptor, PAR-2Antibiotics, AntineoplasticBleomycinReceptor, PAR-2

Identifiers

PMID19226616
PMCPMC3092500
OpenAlexW2089377539

What OpenQuestion holds

Textmetadata
LicenceTDM
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.