ArticleJournal of advanced research2025
Extracellular vesicle-derived miR-146a as a novel crosstalk mechanism for high-fat induced atherosclerosis by targeting SMAD4.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Microfragmented Adipose Tissue in Pain Management: Bridging Regenerative Biology and Clinical Therapeutics.Pain and therapy · 2026Review
- Multi-layer network biology combined with single-cell evidence reveals core regulatory nodes in atherosclerotic plaques and potential drug-targeting directions.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Brazilin attenuates methylglyoxal‑induced endothelial injury by enhancing eIF5A hypusination and inhibiting the AMPK/mTOR‑mediated autophagy/apoptosis axisInternational journal of molecular medicine · 2026Article
- Valorization ofCells · 2026Article
- Endothelial cells modulate immune cell responses during atherosclerosis.Trends in immunology · 2026Review
- Treg-derived exosomal miR-146a orchestrates bidirectional Treg-CAF crosstalk to sustain immunosuppressive tumor microenvironments.Medical oncology (Northwood, London, England) · 2026Review
- Targeting lipophagy in atherosclerosis: Molecular mechanisms, pathogenesis and therapeutic interventions (Review).Molecular medicine reports · 2026Review
- Exosomal miR-4644 Targets SPRY3 to Promote Proliferation and Invasion of Pancreatic Cancer.Cancer medicine · 2026Article
- The Acidic Exosomal miR-1246/WASF3 Axis Regulates Hepatic Stellate Cell Activation and Stiff ECM Remodeling to Promote Pancreatic Ductal Adenocarcinoma Liver Metastasis.International journal of biological sciences · 2026Article
- Electroacupuncture preconditioning alleviates myocardial ischemia-reperfusion injury through reducing the inflammatory response mediated by the miR-146a/TRAF6/IRAK4 pathway.Iranian journal of basic medical sciences · 2026Article
- Integrated experimental and computational insights into the anti-inflammatory potential of flower-derived exosome-like nanoparticles targeting the NF-κB pathway.Frontiers in bioinformatics · 2026Article
- Reduced iron bioavailability drives acute high‑altitude lung injury through HIF1α activation and mitophagy.Molecular medicine reports · 2025Article
- Therapeutic effect of mesenchymal stem cells and their derived exosomes in diseases.Molecular biomedicine · 2025Review
- The role of mitochondrial dysfunction in the pathogenesis of atherosclerosis: A new exploration from bioinformatics analysis.Medicine · 2025Article
- Oleanolic Acid@SPIONs Alleviates Lipid-Oxidative Stress Injury of Zebrafish Blood Vessels via Regulating the Expression of JNK and MAPK Signaling Pathways in Vascular Endothelial Cells.Drug design, development and therapy · 2025Article
- Low-Dose Radiation-Induced Expression of Exosomal miRNAs in the Serum of Medical Radiation Workers.Dose-response : a publication of International Hormesis SocietyArticle
- Quercetin Induces Macrophage Polarization through PI3K-AKT Pathway in Atherosclerosis: Network Pharmacology, Molecule Docking and in vitro Analysis.Iranian journal of pharmaceutical research : IJPRArticle
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionExosome-miR-146a is significantly increased in patients with Atherosclerosis (AS), but its mechanism and effect on AS have not been fully elucidated.
objectivesTo explore the change rule and mechanism of exosomes release, and the role and molecular mechanism of exosome-miR-146a in AS.
methodsWe isolated and identified exosomes from THP-1 macrophages after treating them with ox-LDL. Then used co-immunoprecipitation and silver staining to identify the proteins involved in regulating exosome release. PKH67 was used to label exosomes to confirm that cells can absorb them, and then co-culture with HVSMCs for cell proliferation and migration detection. The target genes of miR-146a were screened and identified through bioinformatics and luciferase activity assay, and the expression of miR-146a and related proteins was detected through qRT-PCR and Western blot in HUVECs. An AS model in LDLR
resultsThe results showed that experimental foam cells from AS showed higher expression of miR-146a. It was observed that NMMHC IIA and HSP70 interacted to regulate the release of exosomes. And HUVECs can absorb exosomes derived from macrophages. In addition, we also found that miR-146a directly targeted the SMAD4 gene to modulate the p38 MAPK signaling pathway, thereby mediating HUVECs damage. Furthermore, exosome-miR-146a induced abnormal proliferation and migration of HVSMCs. The expression of miR-146a was significantly reduced in miR-146a-mimics mice and increased in miR-146a inhibitor mice whereas the inhibition of miR-146a effectively reduced while increasing miR-146a worsened AS in mice.
conclusionOur findings expressed the potential of miR-146a as a favorable therapeutic target for AS, however, further exploration is suggestive for deep understanding of the mechanisms regulating exosome-miR-146a release in vivo and to develop effective therapeutic strategies involving miR-146a.
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