ArticleCellular and molecular life sciences : CMLS2022
Extracellular vesicles carrying proinflammatory factors may spread atherosclerosis to remote locations.
Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 34 citations in OpenAlex.
- THSD7A Exacerbates Atherosclerosis via Activation of Signaling Axis αvβ3/CEBPD/IL1A.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Exosome-Mediated Systemic Signaling: Mechanisms, Disease Integration, and Translational Potential.Current issues in molecular biology · 2026Review
- Extracellular Vesicles in Stroke: Drivers of Brain-Body Network Crosstalk.Translational stroke research · 2026Review
- Reverse cardio-oncology: neuroendocrine axis activation and cardiovascular-disease-derived factors synergistically remodel the tumor microenvironment.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Spinal cord injury-derived exosomes exacerbate damage: miR-155-5p mediates inflammatory responses.Neural regeneration research · 2026Article
- Multifaceted Role of Extracellular Vesicles: Intercellular Messengers to Therapeutic Applications: A Narrative Review.Health science reports · 2026Review
- Atherosclerotic plaque-derived extracellular vesicles mediate smooth muscle cell phenotypic switching and promote vascular remodeling : EVs promote VSMC phenotypic switching.Cellular and molecular life sciences : CMLS · 2026Article
- Research progress on the interaction mechanisms and functions between exosomes and the cytoskeleton.Frontiers in cell and developmental biology · 2026Review
- Myocardium miRNA Analysis Reveals Potential Biomarkers of Sudden Coronary Death in Rats.Current issues in molecular biology · 2025Article
- Extracellular Vesicles as Emerging Regulators in Ischemic and Hypertrophic Cardiovascular Diseases: A Review of Pathogenesis and Therapeutics.Medical science monitor : international medical journal of experimental and clinical research · 2025Review
- Lipid metabolism and lipid signaling in extracellular vesicles ontogeny: from biogenesis to functional execution.Journal of nanobiotechnology · 2025Review
- Carotid Plaque-Derived Small Extracellular Vesicles Mediate Atherosclerosis and Correlate With Plaque Vulnerability.MedComm · 2025Article
- Exosomal non-coding RNAs: key regulators of inflammation-related cardiovascular disorders.European journal of medical research · 2025Review
- Recent advances in the roles of extracellular vesicles in cardiovascular diseases: pathophysiological mechanisms, biomarkers, and cell-free therapeutic strategy.Molecular medicine (Cambridge, Mass.) · 2025Review
- Multi-omics architecture of childhood obesity and metabolic dysfunction uncovers biological pathways and prenatal determinants.Nature communications · 2025Article
- Harnessing extracellular vesicles to tame inflammation: a new strategy for atherosclerosis therapy.Frontiers in immunology · 2025Review
- Emerging understandings of the role of exosomes in atherosclerosis.Journal of cellular physiology · 2025Review
- Macrophage exosomal miR-30c-2-3p in atherosclerotic plaques aggravates microglial neuroinflammation during large-artery atherosclerotic stroke via TGF-β/SMAD2 pathway.Journal of neuroinflammation · 2024Article
- Non-coding RNAs and angiogenesis in cardiovascular diseases: a comprehensive review.Molecular and cellular biochemistry · 2024Review
- Exosome-related gene identification and diagnostic model construction in hepatic ischemia-reperfusion injury.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
20 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most cells involved in atherosclerosis release extracellular vesicles (EVs), which can carry bioactive substances to downstream tissues via circulation. We hypothesized that EVs derived from atherosclerotic plaques could promote atherogenesis in remote locations, a mechanism that mimics the blood metastasis of cancer. Ldlr gene knockout (Ldlr KO) rats were fed on a high cholesterol diet and underwent partial carotid ligation to induce local atherosclerosis. EVs were separated from carotid artery tissues and downstream blood of carotid ligation by centrifugation. MiRNA sequencing and qPCR were then performed to detect miRNA differences in EVs from rats with and without induced carotid atherosclerosis. Biochemical analyses demonstrated that EVs derived from atherosclerosis could increase the expression of ICAM-1, VCAM-1, and E-selectin in endothelial cells in vitro. EVs derived from atherosclerosis contained a higher level of miR-23a-3p than those derived from controls. MiR-23a-3p could promote endothelial inflammation by targeting Dusp5 and maintaining ERK1/2 phosphorylation in vitro. Inhibiting EV release could attenuate atherogenesis and reduce macrophage infiltration in vivo. Intravenously administrating atherosclerotic plaque-derived EVs could induce intimal inflammation, arterial wall thickening and lumen narrowing in the carotids of Ldlr KO rats, while simultaneous injection of miR-23a-3p antagomir could reverse this reaction. The results suggested that EVs may transfer atherosclerosis to remote locations by carrying proinflammatory factors, particularly miR-23a-3p.
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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 Socratic graph.