ArticleCell biology and toxicology2023
MiR-199a-5p-containing macrophage-derived extracellular vesicles inhibit SMARCA4 and alleviate atherosclerosis by reducing endothelial cell pyroptosis.
Article in Cell biology and toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Advances in immune cell-based therapeutic agents for the treatment of inflammation-related diseases.Acta pharmaceutica Sinica. B · 2026Review
- Targeting pyroptosis in atherosclerosis: emerging pharmacologic strategies and natural compound-based therapeutics-a narrative review.International journal of clinical pharmacy · 2026Review
- NLRP3-mediated pyroptosis in cardiovascular disease: from molecular mechanisms to therapeutic targets.Frontiers in pharmacology · 2026Review
- ZDHHC12 Palmitoylates HDAC8 to Promote the Progression of Hepatocellular Carcinoma Associated with a Diet High in Saturated Fatty Acids.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Gene Therapy Approaches for Atherosclerosis Focusing on Targeting Lipid Metabolism and Inflammation.International journal of molecular sciences · 2025Review
- Diversity of extracellular vesicle sources in atherosclerosis: role and therapeutic application.Angiogenesis · 2025Review
- The Crosstalk Between Endothelial Cells, Smooth Muscle Cells, and Macrophages in Atherosclerosis.International journal of molecular sciences · 2025Review
- Exosomes in Atherosclerosis: Role in the Pathogenesis and Targets for Therapy.Current medicinal chemistry · 2025Review
- The relationship between programmed cell death and vascular calcification.Frontiers in cardiovascular medicine · 2025Review
- Macrophage-driven exosomes regulate the progression of cardiovascular disease.Frontiers in pharmacology · 2025Review
- METTL3-mediated m6A modification enhances lncRNA H19 stability to promote endothelial cell inflammation and pyroptosis to aggravate atherosclerosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Extracellular Vesicles as Mediators in Atherosclerotic Cardiovascular Disease.Journal of lipid and atherosclerosis · 2024Review
- Yin-Yang: two sides of extracellular vesicles in inflammatory diseases.Journal of nanobiotechnology · 2024Review
- MicroRNA-19a-3p inhibits endothelial dysfunction in atherosclerosis by targeting JCAD.BMC cardiovascular disorders · 2024Article
- Downregulation of HMGB1 carried by macrophage-derived extracellular vesicles delays atherosclerotic plaque formation through Caspase-11-dependent macrophage pyroptosis.Molecular medicine (Cambridge, Mass.) · 2024Article
- Treatment of Thoracic SMARCA4-Deficient Undifferentiated Tumors: Where We Are and Where We Will Go.International journal of molecular sciences · 2024Review
- MiR-199a-5p Deficiency Promotes Artery Restenosis in Peripheral Artery Disease by Regulating ASMCs FunctionCurrent vascular pharmacology · 2024Article
- Macrophage-derived extracellular vesicles as new players in chronic non-communicable diseases.Frontiers in immunology · 2024Review
- Exosomal Non-Coding RNA Mediates Macrophage Polarization: Roles in Cardiovascular Diseases.Biology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEndothelial cell disturbance underpins a role in pathogenesis of atherosclerosis. Notably, accumulating studies indicate the substantial role of microRNAs (miRs) in atherosclerosis, and miR-199a-5p dysregulation has been associated with atherosclerosis and other cardiovascular disorders. However, the effect of miR-199a-5p on the phenotypes of endothelial cells and atherosclerosis remains largely unknown.
methodsApoE
resultsEVs derived from ox-LDL-induced THP-1-DM expedited inflammation and aorta plaque area in atherosclerotic mice. Besides, miR-199a-5p expression was reduced in EVs from ox-LDL-induced THP-1-DM, and miR-199a-5p inhibition facilitated HAEC pyroptosis and LDH activity. Moreover, miR-199a-5p targeted and restricted SMARCA4, and then SMARCA4 activated the NF-κB pathway by increasing PODXL expression in HAECs.
conclusionEV-packaged inhibited miR-199a-5p from macrophages expedites endothelial cell pyroptosis and further accelerates atherosclerosis through the SMARCA4/PODXL/NF-κB axis, providing promising targets and strategies for the prevention and treatment of atherosclerosis.
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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.