Evidence map›Paper›PMID 31738185›Full record

ArticleThe Journal of clinical investigation2020

Apelin directs endothelial cell differentiation and vascular repair following immune-mediated injury.

Andrew G Masoud, Jiaxin Lin, Abul K Azad, Maikel A Farhan, Conrad Fischer, Lin F Zhu, Hao Zhang, Banu Sis, Zamaneh Kassiri, Ronald B Moore and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 65 citations in OpenAlex.

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  15. Endothelial cell dysfunction in cardiac disease: driver or consequence?Frontiers in cell and developmental biology · 2023
    Review
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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

16 authors at 2 institutions in 1 country.

Andrew G MasoudDepartment of Medicine.
Jiaxin LinDepartment of Surgery.
Abul K AzadDepartment of Medicine.
Maikel A FarhanDepartment of Medicine.
Conrad FischerDepartment of Chemistry, University of Alberta, Edmonton, Alberta, Canada.
Lin F ZhuDepartment of Surgery.
Hao ZhangDepartment of Medicine.
Banu SisDepartment of Laboratory Medicine and Pathology and.
Zamaneh KassiriDepartment of Physiology, University of Alberta, Edmonton, Alberta, Canada.
Ronald B MooreDepartment of Surgery.
Daniel KimDepartment of Medicine.
Colin C AndersonDepartment of Surgery.
John C VederasDepartment of Chemistry, University of Alberta, Edmonton, Alberta, Canada.
Benjamin A AdamDepartment of Laboratory Medicine and Pathology and.
Gavin Y OuditDepartment of Medicine.
Allan G MurrayDepartment of Medicine.
University of Alberta · CACanadian VIGOUR Centre · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sustained, indolent immune injury of the vasculature of a heart transplant limits long-term graft and recipient survival. This injury is mitigated by a poorly characterized, maladaptive repair response. Vascular endothelial cells respond to proangiogenic cues in the embryo by differentiation to specialized phenotypes, associated with expression of apelin. In the adult, the role of developmental proangiogenic cues in repair of the established vasculature is largely unknown. We found that human and minor histocompatibility-mismatched donor mouse heart allografts with alloimmune-mediated vasculopathy upregulated expression of apelin in arteries and myocardial microvessels. In vivo, loss of donor heart expression of apelin facilitated graft immune cell infiltration, blunted vascular repair, and worsened occlusive vasculopathy in mice. In vitro, an apelin receptor agonist analog elicited endothelial nitric oxide synthase activation to promote endothelial monolayer wound repair and reduce immune cell adhesion. Thus, apelin acted as an autocrine growth cue to sustain vascular repair and mitigate the effects of immune injury. Treatment with an apelin receptor agonist after vasculopathy was established markedly reduced progression of arterial occlusion in mice. Together, these initial data identify proangiogenic apelin as a key mediator of coronary vascular repair and a pharmacotherapeutic target for immune-mediated injury of the coronary vasculature.

Indexed as

AnimalsApelinApelin ReceptorsCell DifferentiationCoronary Artery DiseaseEndothelial CellsFemaleHeart TransplantationHumansHuman Umbilical Vein Endothelial CellsInflammationMaleMiceMice, Inbred C57BLMuscle, Smooth, VascularMyocytes, Smooth MuscleApelinApelin ReceptorsNitric Oxide Synthase Type IIICardiologyendothelial cellsTransplantationVasculitis

Identifiers

PMID31738185
PMCPMC6934203
OpenAlexW2984584281

What OpenQuestion holds

Textmetadata
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.