ArticleCirculation research2020
Large Extracellular Vesicle-Associated Rap1 Accumulates in Atherosclerotic Plaques, Correlates With Vascular Risks and Is Involved in Atherosclerosis.
Article in Circulation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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.
The trial behind it
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Identification of PGF+ endothelial cells associated with plaque instability in carotid atherosclerosis by scRNA-seq and RNA-seq analysis.Cell cycle (Georgetown, Tex.) · 2026Article
- Extracellular Vesicles in Cardiovascular Disease: Intercellular Signaling, Liquid Biopsy Biomarkers, and Therapeutic Translation.Circulation research · 2026Review
- Macrophage extracellular traps accelerate atherosclerosis progression via Rap1 pathway-mediated necroptosis and phenotypic switching in vascular smooth muscle cells.Journal of translational medicine · 2026Article
- Article
- High density lipoproteins and extracellular vesicles-distinct but overlapping circulating particles and their role in atherosclerosis.Frontiers in cardiovascular medicine · 2026Review
- Palmitic but Not Oleic Acid Induces Pro-Inflammatory Dysfunction of Human Endothelial Cells from Different Vascular Beds In Vitro.International journal of molecular sciences · 2025Article
- Diversity of extracellular vesicle sources in atherosclerosis: role and therapeutic application.Angiogenesis · 2025Review
- NLRP3, conveyed via extracellular vesicles from metabolic syndrome patients, is involved in atherosclerosis development.Cell communication and signaling : CCS · 2025Article
- Carotid Plaque-Derived Small Extracellular Vesicles Mediate Atherosclerosis and Correlate With Plaque Vulnerability.MedComm · 2025Article
- Recent advances in the roles of extracellular vesicles in cardiovascular diseases: pathophysiological mechanisms, biomarkers, and cell-free therapeutic strategy.Molecular medicine (Cambridge, Mass.) · 2025Review
- Perfluorinated compounds exposure and atherogenic risk characteristics in a high-fat diet condition: In vitro/in vivo models and population panel study.PNAS nexus · 2025Article
- AI-Driven Prediction of Cardio-Oncology Biomarkers Through Protein Corona Analysis.Chemical engineering journal (Lausanne, Switzerland : 1996) · 2025Article
- Stem cell-derived exosome delivery systems for treating atherosclerosis: The new frontier of stem cell therapy.Materials today. Bio · 2025Review
- Mechanism Exploration of Dunyeguanxinning in the Treatment of Atherosclerosis Based on UPLC-Q-Orbitrap HRMS Technology, Network Pharmacology, Molecular Docking and Experimental Validation.Journal of inflammation research · 2025Article
- Circulating extracellular vesicle-carried PTP1B and PP2A phosphatases as regulators of insulin resistance.Diabetologia · 2025Article
- Extracellular Vesicles as Mediators in Atherosclerotic Cardiovascular Disease.Journal of lipid and atherosclerosis · 2024Review
- Bone marrow mesenchymal stem cell-derived extracellular vesicles promote corneal epithelial repair and suppress apoptosis via modulation of Caspase-3 in vitro.FEBS open bio · 2024Article
- Rap1 in the Context of PCSK9, Atherosclerosis, and Diabetes.Current atherosclerosis reports · 2023Review
- Review
- Role of Extracellular Vesicles in the Pathogenesis of Vascular Damage.Hypertension (Dallas, Tex. : 1979) · 2022Review
Corrections and comments
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Authors and funding
22 authors at 4 institutions in 2 countries.
Funding
Abstract
rationaleMetabolic syndrome (MetS) is a cluster of interrelated risk factors for cardiovascular diseases and atherosclerosis. Circulating levels of large extracellular vesicles (lEVs), submicrometer-sized vesicles released from plasma membrane, from MetS patients were shown to induce endothelial dysfunction, but their role in early stage of atherosclerosis and on vascular smooth muscle cells (SMC) remain to be fully elucidated.
objectiveTo determine the mechanisms by which lEVs lead to the progression of atherosclerosis in the setting of MetS. METHODS AND
resultsProteomic analysis revealed that the small GTPase, Rap1 was overexpressed in lEVs from MetS patients compared with those from non-MetS subjects. Rap1 was in GTP-associated active state in both types of lEVs, and Rap1-lEVs levels correlated with increased cardiovascular risks, including stenosis. MetS-lEVs, but not non-MetS-lEVs, increased Rap1-dependent endothelial cell permeability. MetS-lEVs significantly promoted migration and proliferation of human aortic SMC and increased expression of proinflammatory molecules and activation of ERK (extracellular signal-regulated kinase) 5/p38 pathways. Neutralization of Rap1 by specific antibody or pharmacological inhibition of Rap1 completely prevented the effects of lEVs from MetS patients. High-fat diet-fed ApoE
conclusionsThese data demonstrate that Rap1 carried by MetS-lEVs participates in the enhanced SMC proliferation, migration, proinflammatory profile, and activation of ERK5/p38 pathways leading to vascular inflammation and remodeling, and atherosclerosis. These results highlight that Rap1 carried by MetS-lEVs may be a novel determinant of diagnostic value for cardiometabolic risk factors and suggest Rap1 as a promising therapeutic target against the development of atherosclerosis. Graphical Abstract: A graphical abstract is available for this article.
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Registered trials
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.