Evidence map›Paper›PMID 42443923›Full record

ArticleJournal of biomedical science2026

Arginase-2 enhances monocyte-endothelial interaction through regulation of integrin and membrane receptor expression: role in atherogenesis.

Guillaume Ajalbert, Yuejun Yao, Sophie Rohrer, Matteo Caretti, Santhoshkumar Sundaramoorthy, Anastasia Rigkou, Michael Stumpe, Xiu-Fen Ming, Duilio M Potenza, Zhihong Yang

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Article in Journal of biomedical science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Guillaume AjalbertLaboratory of Cardiovascular and Aging Research, Department of Endocrinology, Metabolism, and Cardiovascular System, Faculty of Science and Medicine, University of Fribourg, Chemin du Musee 5, 1700, Fribourg, Switzerland.
Yuejun YaoLaboratory of Cardiovascular and Aging Research, Department of Endocrinology, Metabolism, and Cardiovascular System, Faculty of Science and Medicine, University of Fribourg, Chemin du Musee 5, 1700, Fribourg, Switzerland.
Sophie RohrerLaboratory of Cardiovascular and Aging Research, Department of Endocrinology, Metabolism, and Cardiovascular System, Faculty of Science and Medicine, University of Fribourg, Chemin du Musee 5, 1700, Fribourg, Switzerland.
Matteo CarettiLaboratory of Cardiovascular and Aging Research, Department of Endocrinology, Metabolism, and Cardiovascular System, Faculty of Science and Medicine, University of Fribourg, Chemin du Musee 5, 1700, Fribourg, Switzerland.
Santhoshkumar SundaramoorthyLaboratory of Cardiovascular and Aging Research, Department of Endocrinology, Metabolism, and Cardiovascular System, Faculty of Science and Medicine, University of Fribourg, Chemin du Musee 5, 1700, Fribourg, Switzerland.
Anastasia RigkouLaboratory of Cardiovascular and Aging Research, Department of Endocrinology, Metabolism, and Cardiovascular System, Faculty of Science and Medicine, University of Fribourg, Chemin du Musee 5, 1700, Fribourg, Switzerland.
Michael StumpeDepartment of Biology, University of Fribourg, Chemin du Musee 10, CH-1700, Fribourg, Switzerland.
Xiu-Fen MingLaboratory of Cardiovascular and Aging Research, Department of Endocrinology, Metabolism, and Cardiovascular System, Faculty of Science and Medicine, University of Fribourg, Chemin du Musee 5, 1700, Fribourg, Switzerland.
Duilio M PotenzaLaboratory of Cardiovascular and Aging Research, Department of Endocrinology, Metabolism, and Cardiovascular System, Faculty of Science and Medicine, University of Fribourg, Chemin du Musee 5, 1700, Fribourg, Switzerland. duilio.potenza@unifr.ch.
Zhihong YangLaboratory of Cardiovascular and Aging Research, Department of Endocrinology, Metabolism, and Cardiovascular System, Faculty of Science and Medicine, University of Fribourg, Chemin du Musee 5, 1700, Fribourg, Switzerland. zhihong.yang@unifr.ch.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCirculating monocyte trans-endothelial migration is critical for vascular diseases. The monocyte surface proteins, i.e., integrins and membrane receptors are central in this process. Previous studies demonstrate that ablation of the mitochondrial arginase-2 (ARG2) reduces monocyte/macrophage infiltration in cardiovascular disease. We further investigate whether ARG2 regulates integrin and surface receptor levels in monocytes and facilitates trans-endothelial migration, contributing to atherogenesis.

methodsFor this purpose, human THP1 cells deficient in ARG2 gene (THP1

resultsAs compared to the control THP1

conclusionsOur study identifies ARG2 as a key regulator of monocyte-mediated vascular inflammation and atherogenesis by controlling integrin, chemoattractant receptor expression, and pro-inflammatory cytokine release through TLR4-ERK-NFκB signaling, highlighting ARG2 as a potential therapeutic target for vascular and chronic inflammatory diseases.

Indexed as

ArginaseAtherosclerosisIntegrinsMonocytesReceptors, Cell SurfaceAnimalsHumansMiceMice, KnockoutTHP-1 CellsARG2 protein, humanArginaseIntegrinsReceptors, Cell SurfaceARGINASE 2Endothelial cellsInflammationIntegrinsMonocytes

Identifiers

PMID42443923
PMCPMC13366879

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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.