Evidence map›Paper›PMID 31606133›Full record

ArticleAtherosclerosis2020

Endothelin-1 increases expression and activity of arginase 2 via ETB receptors and is co-expressed with arginase 2 in human atherosclerotic plaques.

Arnar Rafnsson, Ljubica Perisic Matic, Mariette Lengquist, Ali Mahdi, Alexey Shemyakin, Gabrielle Paulsson-Berne, Göran K Hansson, Anders Gabrielsen, Ulf Hedin, Jiangning Yang and 1 more

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Article in Atherosclerosis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Endothelin-1/endothelin B receptor signalling mediates Prx1Journal of orthopaedic translation · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Arnar RafnssonFrom the Department of Medicine, Division of Cardiology, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden. Electronic address: arnar.rafnsson@landspitali.is.
Ljubica Perisic MaticDivision of Vascular Surgery, Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Mariette LengquistDivision of Vascular Surgery, Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Ali MahdiFrom the Department of Medicine, Division of Cardiology, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Alexey ShemyakinFrom the Department of Medicine, Division of Cardiology, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Gabrielle Paulsson-BerneDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine. Karolinska Institutet, Stockholm, Sweden.
Göran K HanssonDivision of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine. Karolinska Institutet, Stockholm, Sweden.
Anders GabrielsenFrom the Department of Medicine, Division of Cardiology, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden; Division of Cardiovascular Medicine, Center for Molecular Medicine, Department of Medicine. Karolinska Institutet, Stockholm, Sweden.
Ulf HedinDivision of Vascular Surgery, Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Jiangning YangFrom the Department of Medicine, Division of Cardiology, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
John PernowFrom the Department of Medicine, Division of Cardiology, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Karolinska Institutet · SEKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsEndothelin-1 (ET-1) and arginase are both suggested to be involved in the inflammatory processes and development of endothelial dysfunction in atherosclerosis. However, information regarding the roles of ET-1 and arginase, as well as the interactions between the two in human atherosclerosis, is scarce. We investigated the expression of ET-1 and its receptors, ET

methodsCarotid plaques and blood samples were retreived from patients undergoing surgery for symptomatic or asymptomatic carotid stenosis. Plaque gene and protein expression was determined and related to clinical characteristics. Functional interactions between ET-1 and arginase were investigated in endothelial cells and THP-1 cells.

resultsExpression of ET-1 and ET

conclusionsThis is the first study that demonstrates co-localization of ET-1 and arginase 2 in human atherosclerotic plaques. ET-1 stimulated arginase 2 expression and activity in endothelial cells, as well as arginase activity and ROS formation in macrophages via an arginase-dependent mechanism. These results indicate an important interaction between the ET pathway and arginase in human atherosclerotic plaques.

Indexed as

ArginaseCells, CulturedEndothelial CellsEndothelin-1HumansPlaque, AtheroscleroticReceptor, Endothelin BARG2 protein, humanArginaseEndothelin-1Receptor, Endothelin BArginaseCarotid artery endarterectomyEndothelial dysfunctionEndothelin-1Endothelin receptor AEndothelin receptor antagonistEndothelin receptor B

Identifiers

PMID31606133
OpenAlexW2979240039

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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.