Evidence map›Paper›PMID 32733273›Full record

ArticleFrontiers in physiology2020

Suppressed Vascular Leakage and Myocardial Edema Improve Outcome From Myocardial Infarction.

Xiujuan Li, Björn Redfors, Miguel Sáinz-Jaspeado, Shujing Shi, Pernilla Martinsson, Narendra Padhan, Margareta Scharin Täng, Jan Borén, Malin Levin, Lena Claesson-Welsh

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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  7. YES to Junctions, No to Src.Nature cardiovascular research · 2022
    Article
  8. Article
  9. Review
  10. Review
  11. The Role of the VEGF Family in Coronary Heart Disease.Frontiers in cardiovascular medicine · 2021
    Review
  12. Article
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 3 institutions in 2 countries.

Xiujuan LiCyrus Tang Hematology Center, Collaborative Innovation Center of Hematology, State Key Laboratory of Radiation Medicine and Protection, Soochow University, Suzhou, China.
Björn RedforsDepartment of Molecular and Clinical Medicine / Wallenberg Laboratory, Institute of Medicine, The Sahlgrenska Academy at University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Miguel Sáinz-JaspeadoBeijer and Science for Life Laboratories, Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
Shujing ShiBeijer and Science for Life Laboratories, Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
Pernilla MartinssonBeijer and Science for Life Laboratories, Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
Narendra PadhanBeijer and Science for Life Laboratories, Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
Margareta Scharin TängDepartment of Molecular and Clinical Medicine / Wallenberg Laboratory, Institute of Medicine, The Sahlgrenska Academy at University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Jan BorénDepartment of Molecular and Clinical Medicine / Wallenberg Laboratory, Institute of Medicine, The Sahlgrenska Academy at University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Malin LevinDepartment of Molecular and Clinical Medicine / Wallenberg Laboratory, Institute of Medicine, The Sahlgrenska Academy at University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Lena Claesson-WelshBeijer and Science for Life Laboratories, Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden.
Uppsala University · SESahlgrenska University Hospital · SEUniversity of Gothenburg · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimThe acute phase of myocardial infarction (MI) is accompanied by edema contributing to tissue damage and disease outcome. Here, we aimed to identify the mechanism whereby vascular endothelial growth factor (VEGF)-A induces myocardial edema in the acute phase of MI to eventually promote development of therapeutics to specifically suppress VEGFA-regulated vascular permeability while preserving collateral vessel formation. METHODS AND

resultsVEGFA regulates vascular permeability and edema by activation of VEGF receptor-2 (VEGFR2), leading to induction of several signaling pathways including the cytoplasmic tyrosine kinase c-Src. The activated c-Src in turn phosphorylates vascular endothelial (VE)-cadherin, leading to dissociation of endothelial adherens junctions. A particular tyrosine at position 949 in mouse VEGFR2 has been shown to be required for activation of c-Src. Wild-type mice and mice with phenylalanine replacing tyrosine (Y) 949 in VEGFR2 (

conclusionSuppression of VEGFA/VEGFR2-regulated vascular permeability leads to diminished edema without affecting vascular density correlating with improved myocardial parameters and survival after MI.

Indexed as

adherens junctionsendothelialmyocardial infarctionvascular permeabilityVE-cadherinVEGF

Identifiers

PMID32733273
PMCPMC7363985
OpenAlexW3040899303

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.