ArticleInternational journal of nanomedicine2020
Honokiol-mesoporous Silica Nanoparticles Inhibit Vascular Restenosis via the Suppression of TGF-β Signaling Pathway.
Article in International journal of nanomedicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Nanoparticle-Based Drug Delivery for Vascular Applications.Bioengineering (Basel, Switzerland) · 2024Review
- Nanoparticle-based approaches for treating restenosis after vascular injury.Frontiers in pharmacology · 2024Review
- Nanosystems in Cardiovascular Medicine: Advancements, Applications, and Future Perspectives.Pharmaceutics · 2023Review
- The Role of TGF-β Signaling in Saphenous Vein Graft Failure after Peripheral Arterial Disease Bypass Surgery.International journal of molecular sciences · 2023Review
- Nanotechnology-Based Drug Delivery Systems for Honokiol: Enhancing Therapeutic Potential and Overcoming Limitations.International journal of nanomedicine · 2023Review
- Molecular Action of Hydroxytyrosol in Attenuation of Intimal Hyperplasia: A Scoping Review.Frontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe main pathological mechanism of restenosis after percutaneous coronary intervention (PCI) is intimal hyperplasia, which is mainly caused by proliferation and migration of vascular smooth muscle cells (VSMCs). Our previous study found that honokiol (HNK), a small-molecule polyphenol, can inhibit neointimal hyperplasia after balloon injury, but its specific mechanism is still unclear. Moreover, poor water solubility as well as low bioavailability of honokiol has limited its practical use.
methodsWe used mesoporous silica nanoparticles (MSNPs) as a standard substance to encapsulate HNK and then assemble into honokiol-mesoporous silica nanoparticles, and we investigated the effect of these nanoparticles on the process of restenosis after common carotid artery injury in rats.
resultsWe report a promising delivery system that loads HNK into MSNPs and finally assembles it into a nanocomposite particle. These HNK-MSNPs not merely inhibited proliferation and migration of VSMCs by reducing phosphorylation of Smad3, but also showed a higher suppression of intimal thickening than the free-honokiol-treated group in a rat model of balloon injury.
conclusionTo sum up, this drug delivery system supplies a potent nano-platform for improving the biological effects of HNK and provides a promising strategy for preventing vascular restenosis.
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