ArticleJournal of the American Heart Association2020
Drug-Eluting Stent Targeting Sp-1-Attenuated Restenosis by Engaging YAP-Mediated Vascular Smooth Muscle Cell Phenotypic Modulation.
Article in Journal of the American Heart Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Hepatitis B Doubly Spliced Protein (HBDSP) Promotes Epithelial-Mesenchymal Transition, Migration, and Invasion via SP1/ETS1-Dependent YAP Activation in Hepatoma Cells.Journal of medical virology · 2026Article
- Knockdown of DVL2 inhibits vascular smooth muscle cell proliferation and migration.Scientific reports · 2026Article
- Unleashing the therapeutic power of verteporfin-eluting stents: modulating YAP signaling to combat carotid artery restenosis and cerebral watershed infarction.Molecular and cellular biochemistry · 2025Article
- YAP/TAZ as mechanobiological signaling pathway in cardiovascular physiological regulation and pathogenesis.Mechanobiology in medicine · 2024Article
- Dihydroartemisinin inhibits restenosis after balloon angioplasty via circHSPA4/miR-19a-5p axis.Molecular and cellular biochemistry · 2024Article
- Sp3 is essential for normal lung morphogenesis and cell cycle progression during mouse embryonic development.Development (Cambridge, England) · 2023Article
- Vascular smooth muscle cells in intimal hyperplasia, an update.Frontiers in physiology · 2022Review
- Global trends and Frontier topics about vascular smooth muscle cells phenotype switch: A bibliometric analysis from 1999 to 2021.Frontiers in pharmacology · 2022Article
- Targeting smooth muscle cell phenotypic switching in vascular disease.JVS-vascular science · 2021Review
- Drug-Eluting Stent Targeting Sp-1-Attenuated Restenosis by Engaging YAP-Mediated Vascular Smooth Muscle Cell Phenotypic Modulation.Journal of the American Heart Association · 2020Article
- Recent advance in treatment of atherosclerosis: Key targets and plaque-positioned delivery strategies.Journal of tissue engineeringReview
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Activation of the YAP (Yes-associated protein) pathway has been demonstrated to be related to smooth muscle cells (SMCs) phenotypic modulation and vessel restenosis. The aim of this study was to illustrate the molecular mechanisms that regulate the expression of YAP during the process of SMCs phenotypic switch. Whether the molecular basis identified in the study could be a potential therapeutic target for drug-eluting stents is further tested. Methods and Results In cell culture and in rat carotid arterial injury models, Sp-1 (specificity protein 1) expression was significantly induced, and correlated with SMCs proliferative phenotype. Overexpression of Sp-1 promoted SMCs proliferation and migration. Conversely, siSp-1 transfection or Sp-1 inhibitor Mithramycin A treatment attenuates SMC proliferation and migration. Through gain- and loss-function assays, we demonstrated that YAP was involved in Sp-1-mediated SMC phenotypic switch. Mechanistically, activated Sp-1 regulated YAP transcriptional expression through binding to its promoter. Moreover, we fabricated a Sp-1 inhibitor Mithramycin A-eluting stent and further tested it. In the rabbit carotid model, Mithramycin A-eluting stent inhibited YAP transcription and attenuated in-stent restenosis through regulating YAP-mediated SMC phenotypic switch. Conclusions Sp-1 controls phenotypic modulation of SMC by regulating transcription factor YAP. Drug-eluting stent targeting Sp-1 might represent a novel therapeutic strategy to prevent in-stent restenosis.
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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.