Evidence map›Paper›PMID 37476204›Full record

ArticleNature cardiovascular research2023

The angiopoietin receptor Tie2 is atheroprotective in arterial endothelium.

Andrey Anisimov, Shentong Fang, Karthik Amudhala Hemanthakumar, Tiit Örd, Kristof van Avondt, Raphael Chevre, Anu Toropainen, Prosanta Singha, Huda Gilani, Su D Nguyen and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Nature cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

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  13. Impaired endothelial function contributes to cardiac dysfunction: role of mitochondrial dynamics.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  14. Article
  15. Acta pharmaceutica Sinica. B · 2024
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 4 institutions in 3 countries.

Andrey Anisimov *Wihuri Research Institute, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland.ORCID https://orcid.org/0000-0003-0259-1273
Shentong Fang *Wihuri Research Institute, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland.ORCID https://orcid.org/0000-0002-3520-7007
Karthik Amudhala HemanthakumarWihuri Research Institute, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland.ORCID https://orcid.org/0000-0001-6151-1005
Tiit ÖrdA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.
Kristof van AvondtInstitute of Experimental Pathology (ExPat), Center of Molecular Biology of Inflammation (ZMBE), University of Münster, Münster, Germany.
Raphael ChevreInstitute of Experimental Pathology (ExPat), Center of Molecular Biology of Inflammation (ZMBE), University of Münster, Münster, Germany.
Anu ToropainenA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.ORCID https://orcid.org/0000-0001-9292-5147
Prosanta SinghaA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.
Huda GilaniA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.
Su D NguyenWihuri Research Institute, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland.
Sinem KaramanWihuri Research Institute, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland.ORCID https://orcid.org/0000-0002-0719-1773
Emilia A KorhonenWihuri Research Institute, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland.
Ralf H AdamsDepartment of Tissue Morphogenesis, Max Planck Institute for Molecular Biomedicine, University of Münster, Münster, Germany.ORCID https://orcid.org/0000-0003-3031-7677
Hellmut G AugustinEuropean Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.ORCID https://orcid.org/0000-0002-7173-4242
Katariina ÖörniWihuri Research Institute, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland.ORCID https://orcid.org/0000-0002-9525-0250
Oliver SoehnleinInstitute of Experimental Pathology (ExPat), Center of Molecular Biology of Inflammation (ZMBE), University of Münster, Münster, Germany.ORCID https://orcid.org/0000-0002-7854-0694
Minna U KaikkonenA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland.ORCID https://orcid.org/0000-0001-6294-0979
Kari AlitaloWihuri Research Institute, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland.ORCID https://orcid.org/0000-0002-7331-0902
University of Helsinki · FIUniversity of Eastern Finland · FIUniversity of Münster · DEGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leukocytes and resident cells in the arterial wall contribute to atherosclerosis, especially at sites of disturbed blood flow. Expression of endothelial Tie1 receptor tyrosine kinase is enhanced at these sites, and attenuation of its expression reduces atherosclerotic burden and decreases inflammation. However, Tie2 tyrosine kinase function in atherosclerosis is unknown. Here we provide genetic evidence from humans and from an atherosclerotic mouse model to show that TIE2 is associated with protection from coronary artery disease. We show that deletion of

Identifiers

PMID37476204
PMCPMC7614785
OpenAlexW4324032702

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.