ArticleJournal of the Royal Society, Interface2015
An in silico study on the role of smooth muscle cell migration in neointimal formation after coronary stenting.
Article in Journal of the Royal Society, Interface, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- A computational model of coronary arteries with in-stent restenosis coupling hemodynamics and pharmacokinetics with growth mechanics.Scientific reports · 2025Article
- Transmission electron microscopy ultrastructural characteristics of the distal middle cerebral artery in moyamoya disease.Scientific reports · 2025Article
- Survivin modulates stiffness-induced vascular smooth muscle cell motility.APL bioengineering · 2025Article
- Cell populations simulated in silico within SimulCell accurately reproduce the behaviour of experimental cell cultures.NPJ systems biology and applications · 2025Article
- Exploring the Potential of Saphenous Vein Grafts Ex Vivo: A Model for Intimal Hyperplasia and Re-Endothelialization.Journal of clinical medicine · 2024Article
- Impact of Tissue Damage and Hemodynamics on Restenosis Following Percutaneous Transluminal Angioplasty: A Patient-Specific Multiscale Model.Annals of biomedical engineering · 2024Article
- Predicting 1-year in-stent restenosis in superficial femoral arteries through multiscale computational modelling.Journal of the Royal Society, Interface · 2023Article
- A predictive multiscale model of in-stent restenosis in femoral arteries: linking haemodynamics and gene expression with an agent-based model of cellular dynamics.Journal of the Royal Society, Interface · 2022Article
- A homogenized constrained mixture model of restenosis and vascular remodelling after balloon angioplasty.Journal of the Royal Society, Interface · 2021Article
- [Review of studies on the biomechanical modelling of the coupling effect between stent degradation and blood vessel remodeling].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2020Article
- Mechanistic evaluation of long-term in-stent restenosis based on models of tissue damage and growth.Biomechanics and modeling in mechanobiology · 2020Article
- Computational modeling for cardiovascular tissue engineering: the importance of including cell behavior in growth and remodeling algorithms.Current opinion in biomedical engineering · 2020Review
- A multiphase model of growth factor-regulated atherosclerotic cap formation.Journal of mathematical biology · 2020Article
- Reversal of Endothelial Extracellular Vesicle-Induced Smooth Muscle Phenotype Transition by Hypercholesterolemia Stimulation: Role of NLRP3 Inflammasome Activation.Frontiers in cell and developmental biology · 2020Article
- Location-Specific Comparison Between a 3D In-Stent Restenosis Model and Micro-CT and Histology Data from Porcine In Vivo Experiments.Cardiovascular engineering and technology · 2019Article
- Mathematical modelling of the restenosis process after stent implantation.Journal of the Royal Society, Interface · 2019Article
- Emerging regulators of vascular smooth muscle cell migration.Journal of muscle research and cell motility · 2019Review
- A versatile hybrid agent-based, particle and partial differential equations method to analyze vascular adaptation.Biomechanics and modeling in mechanobiology · 2019Article
- A cell-based mechanical model of coronary artery tunica media.Journal of the Royal Society, Interface · 2017Article
- A Comparison of Fully-Coupled 3D In-Stent Restenosis Simulations toFrontiers in physiology · 2017Article
Corrections and comments
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Authors and funding
5 authors.
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Abstract
Excessive migration and proliferation of smooth muscle cells (SMCs) has been observed as a major factor contributing to the development of in-stent restenosis after coronary stenting. Building upon the results from in vivo experiments, we formulated a hypothesis that the speed of the initial tissue re-growth response is determined by the early migration of SMCs from the injured intima. To test this hypothesis, a cellular Potts model of the stented artery is developed where stent struts were deployed at different depths into the tissue. An extreme scenario with a ruptured internal elastic lamina was also considered to study the role of severe injury in tissue re-growth. Based on the outcomes, we hypothesize that a deeper stent deployment results in on average larger fenestrae in the elastic lamina, allowing easier migration of SMCs into the lumen. The data also suggest that growth of the neointimal lesions owing to SMC proliferation is strongly dependent on the initial number of migrated cells, which form an initial condition for the later phase of the vascular repair. This mechanism could explain the in vivo observation that the initial rate of neointima formation and injury score are strongly correlated.
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