Evidence map›Paper›PMID 34099640›Full record

ArticleNature communications2021

The C5a/C5a receptor 1 axis controls tissue neovascularization through CXCL4 release from platelets.

Henry Nording, Lasse Baron, David Haberthür, Frederic Emschermann, Matthias Mezger, Manuela Sauter, Reinhard Sauter, Johannes Patzelt, Kai Knoepp, Anne Nording and 17 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 49 citations in OpenAlex.

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  14. Activation of platelets and the complement system in mice withAmerican journal of physiology. Lung cellular and molecular physiology · 2024
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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

27 authors at 10 institutions in 3 countries.

Henry NordingCardioimmunology Group, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany.
Lasse BaronCardioimmunology Group, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany.
David HaberthürInstitute of Anatomy, University of Bern, Bern, Switzerland.ORCID http://orcid.org/0000-0003-3388-9187
Frederic EmschermannUniversity Hospital, Department of Cardiovascular Medicine, Eberhard Karls University, Tübingen, Germany.
Matthias MezgerCardioimmunology Group, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany.
Manuela SauterCardioimmunology Group, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany.
Reinhard SauterCardioimmunology Group, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany.
Johannes PatzeltUniversity Hospital, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany.
Kai KnoeppDepartment of Internal Medicine III, Cardiology, Angiology and Intensive Care Medicine, Martin-Luther-University Halle (Saale), Halle (Saale), Germany.
Anne NordingInstitute of Medical Genetics and Applied Genomics, Eberhard Karls University, Tübingen, Germany.
Moritz MeuselUniversity Hospital, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany.ORCID http://orcid.org/0000-0002-8473-3601
Roza Meyer-SaraeiDZHK (German Centre for Cardiovascular Research), partner site Hamburg/Lübeck/Kiel, Lübeck, Germany.
Ruslan HlushchukInstitute of Anatomy, University of Bern, Bern, Switzerland.
Daniel SeddingDepartment of Internal Medicine III, Cardiology, Angiology and Intensive Care Medicine, Martin-Luther-University Halle (Saale), Halle (Saale), Germany.
Oliver BorstUniversity Hospital, Department of Cardiovascular Medicine, Eberhard Karls University, Tübingen, Germany.
Ingo EitelDZHK (German Centre for Cardiovascular Research), partner site Hamburg/Lübeck/Kiel, Lübeck, Germany.
Christian M KarstenInstitute for Systemic Inflammation Research, University of Lübeck, Lübeck, Germany.
Robert FeilInterfaculty Institute of Biochemistry, University of Tübingen, Tübingen, Germany.ORCID http://orcid.org/0000-0002-7335-4841
Bernd PichlerInstitute for Preclinical Imaging, Eberhard Karls University, Tübingen, Germany.
Jeanette ErdmannDZHK (German Centre for Cardiovascular Research), partner site Hamburg/Lübeck/Kiel, Lübeck, Germany.
Admar VerschoorInstitute for Systemic Inflammation Research, University of Lübeck, Lübeck, Germany.
Emmanouil ChavakisDepartment for Internal Medicine III/Cardiology, University Hospital of the Johann-Wolfgang Goethe University, Frankfurt am Main, Germany.
Triantafyllos ChavakisDepartment of Clinical Pathobiochemistry, Institute of Clinical Chemistry and Laboratory Medicine, Medical Faculty, Technische Universität Dresden, Dresden, Germany.ORCID http://orcid.org/0000-0002-1869-5141
Philipp von HundelshausenInstitute for Cardiovascular Prevention, Ludwig Maximilians University Munich, Munich, Germany.
Jörg KöhlInstitute for Systemic Inflammation Research, University of Lübeck, Lübeck, Germany.ORCID http://orcid.org/0000-0003-1121-3178
Meinrad GawazUniversity Hospital, Department of Cardiovascular Medicine, Eberhard Karls University, Tübingen, Germany.ORCID http://orcid.org/0000-0003-1124-9592
Harald F LangerCardioimmunology Group, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany. harald.langer@uksh.de.ORCID http://orcid.org/0000-0003-2224-0518
University of Lübeck · DEUniversity of Tübingen · DEGerman Centre for Cardiovascular Research · DEMartin Luther University Halle-Wittenberg · DEUniversity of Bern · CHCincinnati Children's Hospital Medical Center · USGoethe University Frankfurt · DELudwig-Maximilians-Universität München · DETechnische Universität Dresden · DEUniversity Hospital Schleswig-Holstein · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Platelets contribute to the regulation of tissue neovascularization, although the specific factors underlying this function are unknown. Here, we identified the complement anaphylatoxin C5a-mediated activation of C5a receptor 1 (C5aR1) on platelets as a negative regulatory mechanism of vessel formation. We showed that platelets expressing C5aR1 exert an inhibitory effect on endothelial cell functions such as migration and 2D and 3D tube formation. Growth factor- and hypoxia-driven vascularization was markedly increased in C5ar1

Indexed as

Angiogenesis Inducing AgentsAnimalsBlood PlateletsComplement ActivationComplement C5aInflammationMiceMice, KnockoutPlatelet Factor 4Receptor, Anaphylatoxin C5aReceptors, CXCR3Signal TransductionAngiogenesis Inducing AgentsC5ar1 protein, mouseComplement C5aCxcr3 protein, mousePlatelet Factor 4Receptor, Anaphylatoxin C5aReceptors, CXCR3

Identifiers

PMID34099640
PMCPMC8185003
OpenAlexW3172911545

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.