Evidence map›Paper›PMID 34218201›Full record

ArticleRedox biology2021

The hydrogen-peroxide producing NADPH oxidase 4 does not limit neointima development after vascular injury in mice.

Giulia K Buchmann, Christoph Schürmann, Manuela Spaeth, Wesley Abplanalp, Lukas Tombor, David John, Timothy Warwick, Flávia Rezende, Andreas Weigert, Ajay M Shah and 5 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 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
0.7field-weighted citation impact, top 32% 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, 12 citations in OpenAlex.

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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

15 authors at 5 institutions in 2 countries.

Giulia K BuchmannInstitute for Cardiovascular Physiology, Goethe-University, Frankfurt Am Main, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhein Main, Frankfurt Am Main, Germany.
Christoph SchürmannInstitute for Cardiovascular Physiology, Goethe-University, Frankfurt Am Main, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhein Main, Frankfurt Am Main, Germany.
Manuela SpaethInstitute for Cardiovascular Physiology, Goethe-University, Frankfurt Am Main, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhein Main, Frankfurt Am Main, Germany.
Wesley AbplanalpGerman Center for Cardiovascular Research (DZHK), Partner Site Rhein Main, Frankfurt Am Main, Germany; Institute of Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt, Germany.
Lukas TomborGerman Center for Cardiovascular Research (DZHK), Partner Site Rhein Main, Frankfurt Am Main, Germany; Institute of Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt, Germany.
David JohnGerman Center for Cardiovascular Research (DZHK), Partner Site Rhein Main, Frankfurt Am Main, Germany; Institute of Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt, Germany.
Timothy WarwickInstitute for Cardiovascular Physiology, Goethe-University, Frankfurt Am Main, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhein Main, Frankfurt Am Main, Germany.
Flávia RezendeInstitute for Cardiovascular Physiology, Goethe-University, Frankfurt Am Main, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhein Main, Frankfurt Am Main, Germany.
Andreas WeigertInstitute of Biochemistry I, Faculty of Medicine, Goethe-University Frankfurt, Frankfurt, Germany.
Ajay M ShahSchool of Cardiovascular Medicine & Sciences, King's College London, British Heart Foundation Centre, London, UK.
Martin-Leo HansmannDepartment of Pathology, University Hospital Frankfurt, Germany.
Norbert WeissmannExcellence Cluster Cardio-Pulmonary Institute (CPI), Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Center for Lung Research (DZL), Gießen, Germany.
Stefanie DimmelerGerman Center for Cardiovascular Research (DZHK), Partner Site Rhein Main, Frankfurt Am Main, Germany; Institute of Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University Frankfurt, Germany.
Katrin SchröderInstitute for Cardiovascular Physiology, Goethe-University, Frankfurt Am Main, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhein Main, Frankfurt Am Main, Germany.
Ralf P BrandesInstitute for Cardiovascular Physiology, Goethe-University, Frankfurt Am Main, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhein Main, Frankfurt Am Main, Germany. Electronic address: brandes@vrc.uni-frankfurt.de.
German Centre for Cardiovascular Research · DEGoethe University Frankfurt · DEBritish Heart Foundation · GBCardio-Pulmonary Institute · DEUniversity Hospital Frankfurt · DE

Funding

British Heart Foundation CH/1999001/11735
6 · The paper itself

Abstract

objectiveThe NADPH oxidase Nox4 is an important source of H METHODS AND

resultsGenetic deletion of Nox4 by a tamoxifen-activated Cre-Lox-system did not impact on neointima formation in the carotid artery wire injury model. To understand this unexpected finding, time-resolved single-cell RNA-sequencing (scRNAseq) from injured carotid arteries of control mice and massive-analysis-of-cDNA-ends (MACE)-RNAseq from the neointima harvested by laser capture microdissection of control and Nox4 knockout mice was performed. This revealed that resting smooth muscle cells (SMCs) and fibroblasts exhibit high Nox4 expression, but that the proliferating de-differentiated SMCs, which give rise to the neointima, have low Nox4 expression. In line with this, the first weeks after injury, gene expression was unchanged between the carotid artery neointimas of control and Nox4 knockout mice.

conclusionUpon vascular injury, Nox4 expression is transiently lost in the cells which comprise the neointima. NADPH oxidase 4 therefore does not interfere with restenosis development after wire-induced vascular injury.

Indexed as

NADPH Oxidase 4NeointimaVascular System InjuriesAnimalsCells, CulturedHydrogen PeroxideMiceMice, KnockoutMyocytes, Smooth MuscleHydrogen PeroxideNADPH Oxidase 4Nox4 protein, mouseCarotid injuryInflammationNADPH oxidaseNox4Reactive oxygen speciesRestenosisSingle-cell RNA sequencing

Identifiers

PMID34218201
PMCPMC8256285
OpenAlexW3175693298

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.