Evidence map›Paper›PMID 30632166›Full record

ArticleThe Journal of pathology2019

Neutrophil elastase plays a non-redundant role in remodeling the venular basement membrane and neutrophil diapedesis post-ischemia/reperfusion injury.

Mathieu-Benoit Voisin, Giovanna Leoni, Abigail Woodfin, Laure Loumagne, Nimesh Sa Patel, Rosanna Di Paola, Salvatore Cuzzocrea, Christoph Thiemermann, Mauro Perretti, Sussan Nourshargh

Open access · hybridAbstract read
In one paragraph

Article in The Journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 43 citations in OpenAlex.

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  15. Neutrophil degranulation and myocardial infarction.Cell communication and signaling : CCS · 2022
    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

10 authors at 2 institutions in 3 countries.

Mathieu-Benoit VoisinWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.ORCID 0000-0003-3001-0894
Giovanna LeoniWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Abigail WoodfinWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Laure LoumagneWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Nimesh Sa PatelWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Rosanna Di PaolaDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy.
Salvatore CuzzocreaDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy.
Christoph ThiemermannWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Mauro PerrettiWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Sussan NoursharghWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Queen Mary University of London · GBUniversity of Messina · IT

Funding

Arthritis Research UK 19913British Heart Foundation FS/05/078/19406British Heart Foundation FS/11/19/28761British Heart Foundation PG/03/123/16102Versus Arthritis 19913Wellcome TrustWellcome Trust 098291/Z/12/ZWellcome Trust 101604/Z/13/Z
6 · The paper itself

Abstract

Ischemia/reperfusion (I/R) injury is a severe inflammatory insult associated with numerous pathologies, such as myocardial infarction, stroke and acute kidney injury. I/R injury is characterized by a rapid influx of activated neutrophils secreting toxic free radical species and degrading enzymes that can irreversibly damage the tissue, thus impairing organ functions. Significant efforts have been invested in identifying therapeutic targets to suppress neutrophil recruitment and activation post-I/R injury. In this context, pharmacological targeting of neutrophil elastase (NE) has shown promising anti-inflammatory efficacy in a number of experimental and clinical settings of I/R injury and is considered a plausible clinical strategy for organ care. However, the mechanisms of action of NE, and hence its inhibitors, in this process are not fully understood. Here we conducted a comprehensive analysis of the impact of NE genetic deletion on neutrophil infiltration in four murine models of I/R injury as induced in the heart, kidneys, intestine and cremaster muscle. In all models, neutrophil migration into ischemic regions was significantly suppressed in NE

Indexed as

AnimalsBasement MembraneDisease Models, AnimalGene DeletionKidneyLeukocyte ElastaseMaleMice, Inbred C57BLMice, KnockoutMicroscopy, ConfocalMyocardial Reperfusion InjuryNeutrophil InfiltrationNeutrophilsReperfusion InjuryTransendothelial and Transepithelial MigrationVascular RemodelingLeukocyte Elastaseelastaseischemia/reperfusion injuryneutrophilvenular basement membrane

Identifiers

PMID30632166
PMCPMC6850085
OpenAlexW2910308593

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.