Evidence map›Paper›PMID 31636306›Full record

ArticleScientific reports2019

PKM2 regulates endothelial cell junction dynamics and angiogenesis via ATP production.

Jesús Gómez-Escudero, Cristina Clemente, Diego García-Weber, Rebeca Acín-Pérez, Jaime Millán, José A Enríquez, Katie Bentley, Peter Carmeliet, Alicia G Arroyo

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

40 citing papers in PubMed, 54 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

9 authors at 6 institutions in 6 countries.

Jesús Gómez-EscuderoVascular Pathophysiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC). Melchor Fernández Almagro 3, 28029, Madrid, Spain.
Cristina ClementeVascular Pathophysiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC). Melchor Fernández Almagro 3, 28029, Madrid, Spain.
Diego García-WeberCentro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas (CSIC), Universidad Autónoma de Madrid, 28049, Madrid, Spain.
Rebeca Acín-PérezMyocardial Pathology Areas, Centro Nacional de Investigaciones Cardiovasculares (CNIC). Melchor Fernández Almagro 3, 28029, Madrid, Spain.
Jaime MillánCentro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas (CSIC), Universidad Autónoma de Madrid, 28049, Madrid, Spain.
José A EnríquezMyocardial Pathology Areas, Centro Nacional de Investigaciones Cardiovasculares (CNIC). Melchor Fernández Almagro 3, 28029, Madrid, Spain.ORCID http://orcid.org/0000-0002-3671-2961
Katie BentleyComputational Biology Laboratory, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Peter CarmelietLaboratory of Angiogenesis and Vascular Metabolism, Center for Cancer Biology, Vlaams Instituut voor Biotechnologie (VIB), B-3000, Leuven, Belgium.
Alicia G ArroyoVascular Pathophysiology, Centro Nacional de Investigaciones Cardiovasculares (CNIC). Melchor Fernández Almagro 3, 28029, Madrid, Spain. agarroyo@cib.csic.es.ORCID http://orcid.org/0000-0002-1536-3846
Spanish National Centre for Cardiovascular Research · ESConsejo Superior de Investigaciones Científicas · ESQueen Mary University of London · GBSpanish National Centre for Cardiovascular Research · ESSun Yat-sen University · CNUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis, the formation of new blood vessels from pre-existing ones, occurs in pathophysiological contexts such as wound healing, cancer, and chronic inflammatory disease. During sprouting angiogenesis, endothelial tip and stalk cells coordinately remodel their cell-cell junctions to allow collective migration and extension of the sprout while maintaining barrier integrity. All these processes require energy, and the predominant ATP generation route in endothelial cells is glycolysis. However, it remains unclear how ATP reaches the plasma membrane and intercellular junctions. In this study, we demonstrate that the glycolytic enzyme pyruvate kinase 2 (PKM2) is required for sprouting angiogenesis in vitro and in vivo through the regulation of endothelial cell-junction dynamics and collective migration. We show that PKM2-silencing decreases ATP required for proper VE-cadherin internalization/traffic at endothelial cell-cell junctions. Our study provides fresh insight into the role of ATP subcellular compartmentalization in endothelial cells during angiogenesis. Since manipulation of EC glycolysis constitutes a potential therapeutic intervention route, particularly in tumors and chronic inflammatory disease, these findings may help to refine the targeting of endothelial glycolytic activity in disease.

Indexed as

Neovascularization, PhysiologicAdenosine TriphosphateAnimalsAntigens, CDCadherin 5CadherinsCarrier ProteinsCell MovementEndocytosisGene SilencingHumansHuman Umbilical Vein Endothelial CellsIntercellular JunctionsMembrane ProteinsMice, Inbred C57BLPseudopodiaAdenosine TriphosphateAntigens, CDCadherin 5CadherinsCarrier ProteinsMembrane ProteinsPkm protein, mousePyruvate KinaseThyroid Hormone-Binding ProteinsThyroid Hormones

Identifiers

PMID31636306
PMCPMC6803685
OpenAlexW2980895027

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.