ArticleCell communication and signaling : CCS2022
Endothelial colony-forming cell-derived exosomal miR-21-5p regulates autophagic flux to promote vascular endothelial repair by inhibiting SIPL1A2 in atherosclerosis.
Article in Cell communication and signaling : CCS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.
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Who cites it
31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 41 citations in OpenAlex.
- Advances in the study of exosomes in cardiovascular diseases.Journal of advanced research · 2024Pooled it
- A bibliometric analysis of exosomes in aging from 2007 to 2023.Frontiers in medicine · 2024Pooled it
- Review
- A high-performance hydrogel platform enabling dual anti-miR-21 and TGF-β1 delivery to improve arterial plaque stability and enhance therapeutic angiogenesis outcomes.Scientific reports · 2026Article
- From Cerebrovascular Injury to Vascular Cognitive Impairment and Dementia: Therapeutic Potential of Stem Cell-Derived Extracellular Vesicles.Biomedicines · 2026Review
- Nanoscale Delivery of MicroRNAs via Extracellular Vesicles: Mechanisms Potential in Modulating Cellular Senescence.International journal of nanomedicine · 2026Review
- Establishing an atherosclerosis diagnostic model based on WGCNA and machine learning algorithms with key genes in cholesterol metabolism and ferroptosis, and revealing the regulatory role of HMOX1 in cellular ferroptosis.Frontiers in cardiovascular medicine · 2026Article
- Harnessing Natural Extracellular Vesicles to Combat Age-Related Diseases: From Aging Drivers to Therapeutic Opportunities.International journal of nanomedicine · 2026Review
- Exosomal miRNAs: A New Frontier in Cardiovascular Disease Diagnosis and Treatment.Journal of cardiovascular translational research · 2025Review
- Diversity of extracellular vesicle sources in atherosclerosis: role and therapeutic application.Angiogenesis · 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
- Blood-Brain Barrier (BBB) Dysfunction in CNS Diseases: Paying Attention to Pericytes.CNS neuroscience & therapeutics · 2025Review
- Unlocking the Potential of Extracellular Vesicles in Cardiovascular Disease.Journal of cellular and molecular medicine · 2025Review
- Cardiovascular diseases in the elderly: possibilities for modulating autophagy using non-coding RNAs.Frontiers in cell and developmental biology · 2025Review
- Global research trends on exosomes in atherosclerosis: a bibliometric and scientometric analysis (2004-2025).Frontiers in cardiovascular medicine · 2025Article
- Extracellular vesicles in cardiovascular diseases: pathogenic mediators, diagnostic tools, and therapeutic vectors.Frontiers in cardiovascular medicine · 2025Review
- Engineered biomimetic nanovesicles-laden multifunctional hydrogel enhances targeted therapy of diabetic wound.Materials today. Bio · 2024Article
- Article
- Endothelial progenitor cell-derived extracellular vesicles: the world of potential prospects for the treatment of cardiovascular diseases.Cell & bioscience · 2024Review
- MicroRNA-142-3p alleviated high salt-induced cardiac fibrosis via downregulating optineurin-mediated mitophagy.iScience · 2024Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPercutaneous transluminal coronary angioplasty (PTCA) represents an efficient therapeutic method for atherosclerosis but conveys a risk of causing restenosis. Endothelial colony-forming cell-derived exosomes (ECFC-exosomes) are important mediators during vascular repair. This study aimed to investigate the therapeutic effects of ECFC-exosomes in a rat model of atherosclerosis and to explore the molecular mechanisms underlying the ECFC-exosome-mediated effects on ox-LDL-induced endothelial injury.
methodsThe effect of ECFC-exosome-mediated autophagy on ox-LDL-induced human microvascular endothelial cell (HMEC) injury was examined by cell counting kit-8 assay, scratch wound assay, tube formation assay, western blot and the Ad-mCherry-GFP-LC3B system. RNA-sequencing assays, bioinformatic analysis and dual-luciferase reporter assays were performed to confirm the interaction between the miR-21-5p abundance of ECFC-exosomes and SIPA1L2 in HMECs. The role and underlying mechanism of ECFC-exosomes in endothelial repair were explored using a high-fat diet combined with balloon injury to establish an atherosclerotic rat model of vascular injury. Evans blue staining, haematoxylin and eosin staining and western blotting were used to evaluate vascular injury.
resultsECFC-exosomes were incorporated into HMECs and promoted HMEC proliferation, migration and tube formation by repairing autophagic flux and enhancing autophagic activity. Subsequently, we demonstrated that miR-21-5p, which is abundant in ECFC-exosomes, binds to the 3' untranslated region of SIPA1L2 to inhibit its expression, and knockout of miR-21-5p in ECFC-exosomes reversed ECFC-exosome-decreased SIPA1L2 expression in ox-LDL-induced HMEC injury. Knockdown of SIPA1L2 repaired autophagic flux and enhanced autophagic activity to promote cell proliferation in ox-LDL-treated HMECs. ECFC-exosome treatment attenuated vascular endothelial injury, regulated lipid balance and activated autophagy in an atherogenic rat model of vascular injury, whereas these effects were eliminated with ECFC-exosomes with knockdown of miR-21-5p.
conclusionsOur study demonstrated that ECFC-exosomes protect against atherosclerosis- or PTCA-induced vascular injury by rescuing autophagic flux and inhibiting SIAP1L2 expression through delivery of miR-21-5p. Video Abstract.
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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.