Evidence map›Paper›PMID 40517251›Full record

ArticleCell communication and signaling : CCS2025

NLRP3, conveyed via extracellular vesicles from metabolic syndrome patients, is involved in atherosclerosis development.

Xavier Vidal-Gómez, Luisa Vergori, Séverine Dubois, Frédéric Gagnadoux, Samir Henni, Reuben Veerapen, Olivier Meilhac, Mercedes Muñoz-Picos, Concepción Peiró, M Carmen Martinez and 2 more

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Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

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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

5 citing papers in PubMed.

  1. Article
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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

12 authors.

Xavier Vidal-GómezPhyMedExp, University of Montpellier, INSERM, CNRS, Montpellier, France.ORCID http://orcid.org/0000-0002-7640-7996
Luisa VergoriSOPAM, INSERM U1063, UNIV Angers, SFR ICAT, Angers, France.
Séverine DuboisCHU d'Angers, Angers, France.
Frédéric GagnadouxSOPAM, INSERM U1063, UNIV Angers, SFR ICAT, Angers, France.ORCID http://orcid.org/0000-0002-4231-5102
Samir HenniCHU d'Angers, Angers, France.
Reuben VeerapenGroupe Clinifutur, Clinique Sainte-Clotilde, Sainte-Clotilde, France.
Olivier MeilhacDéTROI, INSERM U1188, Université de La Réunion, La Réunion, France.
Mercedes Muñoz-PicosSOPAM, INSERM U1063, UNIV Angers, SFR ICAT, Angers, France.ORCID http://orcid.org/0000-0002-1679-9588
Concepción PeiróDepartment of Pharmacology, Medicine School, Autonomous University of Madrid, Madrid, Spain.ORCID http://orcid.org/0000-0002-9690-7816
M Carmen MartinezPhyMedExp, University of Montpellier, INSERM, CNRS, Montpellier, France.ORCID http://orcid.org/0000-0003-3897-7397
Ramaroson AndriantsitohainaPhyMedExp, University of Montpellier, INSERM, CNRS, Montpellier, France. ramaroson.andriantsitohaina@inserm.fr.ORCID http://orcid.org/0000-0002-4770-3585
Metabol Study Group

Funding

Fondation pour la Recherche Médicale SPF201809006985
6 · The paper itself

Abstract

backgroundInappropriate activation of the Nod-like receptor protein 3 (NLRP3)-inflammasome contributes to atherosclerosis progression and plaque instability in patients with cardiovascular events. However, its role in the atherosclerosis is not fully understood. We sought to uncover actionable targets that could help to refine the diagnostic values of metabolic syndrome (MetS) patients by taking advantage of extracellular vesicles (EVs) to support the inflammatory hypothesis of atherosclerosis.

methodsCirculating large (lEVs) and small (sEVs) EVs from non-MetS subjects and MetS patients were isolated and characterized. The involvement of NLRP3 in the effects of EVs on human aortic endothelial and smooth muscle cells (SMC) and macrophages were analyzed. The pathological relevance in human atherosclerotic lesions was investigated.

resultsCirculating levels of lEVs carrying NLRP3 correlated with metabolic risk factors associated with obesity and insulin resistance. Both types of EVs from MetS patients increased endothelial permeability, monocyte transmigration, SMC migration and secretion of pro-inflammatory molecules by monocyte/macrophages. Interestingly, MetS-lEVs, but not MetS-sEVs, increased SMC proliferation and IL-1ß production. EVs isolated from advanced human plaques demonstrated an accumulation of EVs carrying NLRP3 and their implication in endothelial permeability increase. Pharmacological inhibition of NLRP3-inflammasome carried by MetS-EVs prevented all the effects leading to vascular inflammation and remodeling.

conclusionsOur data demonstrate that NLRP3-inflammasome, carried by EVs, is actively involved in vascular inflammation and atherosclerosis development in MetS. We highlight NLRP3 carried by EVs as potential biomarker and target for potential therapeutic strategies of atherosclerosis-related diseases leading to major adverse cardiovascular events.

Indexed as

AtherosclerosisExtracellular VesiclesMetabolic SyndromeNLR Family, Pyrin Domain-Containing 3 ProteinEndothelial CellsFemaleHumansInflammasomesMacrophagesMaleMiddle AgedMyocytes, Smooth MuscleInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanAtherosclerosis developmentExtracellular vesiclesMetabolic syndromeNLRP3Vascular inflammation

Identifiers

PMID40517251
PMCPMC12167584

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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.