Evidence map›Paper›PMID 32681081›Full record

ArticleNature communications2020

Preservation of microvascular barrier function requires CD31 receptor-induced metabolic reprogramming.

Kenneth C P Cheung, Silvia Fanti, Claudio Mauro, Guosu Wang, Anitha S Nair, Hongmei Fu, Silvia Angeletti, Silvia Spoto, Marta Fogolari, Francesco Romano and 11 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. 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
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

37 citing papers in PubMed, 62 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

21 authors at 5 institutions in 4 countries.

Kenneth C P Cheung *William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.ORCID http://orcid.org/0000-0002-7783-1780
Silvia Fanti *William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.
Claudio MauroWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.ORCID http://orcid.org/0000-0002-3736-0099
Guosu WangWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.
Anitha S NairWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.
Hongmei FuWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.
Silvia AngelettiUnit of Clinical Laboratory Science, University Campus Bio-Medico of Rome, Rome, Italy.
Silvia SpotoInternal Medicine Department, University campus Bio-Medico of Rome, Rome, Italy.ORCID http://orcid.org/0000-0002-8799-4997
Marta FogolariUnit of Clinical Laboratory Science, University Campus Bio-Medico of Rome, Rome, Italy.ORCID http://orcid.org/0000-0002-0218-5884
Francesco RomanoUnit of Clinical Laboratory Science, University Campus Bio-Medico of Rome, Rome, Italy.
Dunja AksentijevicSchool of Biological and Chemical Sciences, Queen Mary University of London, Mile End Road, London, E1 4NS, UK.ORCID http://orcid.org/0000-0002-8480-6727
Weiwei LiuDepartment of Head and Neck Surgery, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangzhou, 510060, People's Republic of China.
Baiying LiSchool of Life Sciences, Centre for Cell & Developmental Biology and Partner State Key Laboratory of Agrobiotechnology, The Chinese University of Hong Kong, Hong Kong SAR, China.
Lixin ChengSchool of Life Sciences, Centre for Cell & Developmental Biology and Partner State Key Laboratory of Agrobiotechnology, The Chinese University of Hong Kong, Hong Kong SAR, China.ORCID http://orcid.org/0000-0002-9427-383X
Liwen JiangSchool of Life Sciences, Centre for Cell & Developmental Biology and Partner State Key Laboratory of Agrobiotechnology, The Chinese University of Hong Kong, Hong Kong SAR, China.
Juho VuononvirtaWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.ORCID http://orcid.org/0000-0003-0776-601X
Thanushiyan R PoobalasingamWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.
David M SmithAstraZeneca R&D, Cambridge Science Park, Milton Road, Cambridge, CB4 0WG, UK.ORCID http://orcid.org/0000-0001-6831-280X
Massimo CiccozziUnit of Medical Statistic and Molecular Epidemiology, University Campus Bio-Medico of Rome, Rome, Italy.ORCID http://orcid.org/0000-0003-3866-9239
Egle Solito *William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.ORCID http://orcid.org/0000-0001-5279-0049
Federica M Marelli-Berg *William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK. f.marelli-berg@qmul.ac.uk.ORCID http://orcid.org/0000-0001-8747-5823
Queen Mary University of London · GBUniversità Campus Bio-Medico · ITChinese University of Hong Kong · HKAstraZeneca (United Kingdom) · GBSun Yat-sen University · CN

Funding

British Heart Foundation CH/15/2/32064British Heart Foundation FS/11/64/2894British Heart Foundation FS/12/38/29640British Heart Foundation RG/14/2/30616Medical Research Council MR/P021220/1
6 · The paper itself

Abstract

Endothelial barrier (EB) breaching is a frequent event during inflammation, and it is followed by the rapid recovery of microvascular integrity. The molecular mechanisms of EB recovery are poorly understood. Triggering of MHC molecules by migrating T-cells is a minimal signal capable of inducing endothelial contraction and transient microvascular leakage. Using this model, we show that EB recovery requires a CD31 receptor-induced, robust glycolytic response sustaining junction re-annealing. Mechanistically, this response involves src-homology phosphatase activation leading to Akt-mediated nuclear exclusion of FoxO1 and concomitant β-catenin translocation to the nucleus, collectively leading to cMyc transcription. CD31 signals also sustain mitochondrial respiration, however this pathway does not contribute to junction remodeling. We further show that pathologic microvascular leakage in CD31-deficient mice can be corrected by enhancing the glycolytic flux via pharmacological Akt or AMPK activation, thus providing a molecular platform for the therapeutic control of EB response.

Indexed as

Animalsbeta CateninEndothelial CellsFemaleForkhead Box Protein O1MaleMiceMicrovesselsPlatelet Endothelial Cell Adhesion Molecule-1Proto-Oncogene Proteins c-aktSignal Transductionbeta CateninForkhead Box Protein O1Platelet Endothelial Cell Adhesion Molecule-1Proto-Oncogene Proteins c-akt

Identifiers

PMID32681081
PMCPMC7367815
OpenAlexW3043128340

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.