Neointimal Hyperplasia: Basic Considerations

Model, Lynn; Dardik, Alan

doi:10.1002/9781118481370.ch10

Cited by 4 publications

(6 citation statements)

References 142 publications

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“…A next extension of this part of the model might consider additional types of cells contributing to NIH (e.g., fibroblasts, macrophages) (Model and Dardik, 2012). …”

Section: Discussionmentioning

confidence: 99%

“…Results from the multi-scale approach using the biochemical model proposed in this paper are very encouraging even if only one type of cells was considered, i.e., smooth muscle cells. A next extension of this part of the model might consider additional types of cells contributing to NIH (e.g., fibroblasts, macrophages) (Model and Dardik, 2012 ).…”

Section: Discussionmentioning

confidence: 99%

“…After injury, the start of the inflammatory process causes them to migrate from the media to the intima, accumulating there and causing the intima to thicken (Kohler, 2005; Model and Dardik, 2012). …”

Section: Methodsmentioning

confidence: 99%

“…This model considers smooth muscle cells proliferation in the intima to be the most critical response from vascular tissue after injury to the endothelium (Boyle et al, 2010 ; Model and Dardik, 2012 ). After injury, the start of the inflammatory process causes them to migrate from the media to the intima, accumulating there and causing the intima to thicken (Kohler, 2005 ; Model and Dardik, 2012 ).…”

Section: Methodsmentioning

confidence: 99%

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Patient-Specific, Multi-Scale Modeling of Neointimal Hyperplasia in Vein Grafts

et al. 2017

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Neointimal hyperplasia is amongst the major causes of failure of bypass grafts. The disease progression varies from patient to patient due to a range of different factors. In this paper, a mathematical model will be used to understand neointimal hyperplasia in individual patients, combining information from biological experiments and patient-specific data to analyze some aspects of the disease, particularly with regard to mechanical stimuli due to shear stresses on the vessel wall. By combining a biochemical model of cell growth and a patient-specific computational fluid dynamics analysis of blood flow in the lumen, remodeling of the blood vessel is studied by means of a novel computational framework. The framework was used to analyze two vein graft bypasses from one patient: a femoro-popliteal and a femoro-distal bypass. The remodeling of the vessel wall and analysis of the flow for each case was then compared to clinical data and discussed as a potential tool for a better understanding of the disease. Simulation results from this first computational approach showed an overall agreement on the locations of hyperplasia in these patients and demonstrated the potential of using new integrative modeling tools to understand disease progression.

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“…A next extension of this part of the model might consider additional types of cells contributing to NIH (e.g., fibroblasts, macrophages) (Model and Dardik, 2012). …”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Patient-Specific, Multi-Scale Modeling of Neointimal Hyperplasia in Vein Grafts

et al. 2017

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“…Vascular restenosis is a common complication of percutaneous transluminal coronary angioplasty (PTCA) and stent implantation, which severely compromises the efficacy of treatment. Despite improvements in technology, the incidence of restenosis remains high due to neointimal hyperplasia, which results from mechanical dilating injuries and may be augmented by the presence of the stent (1). Under these circumstances, the supplementation of pharmacological treatments limiting neointimal ingrowth may improve the therapeutic outcomes.…”

Section: Introductionmentioning

confidence: 99%

Lycopene inhibits neointimal hyperplasia through regulating lipid metabolism and suppressing oxidative stress

Mao

Liu

et al. 2014

Molecular Medicine Reports

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The present study aimed to investigate the possible mechanism(s) through which lycopene inhibits neointimal hyperplasia in restenosis models. A total of 32 white rabbits were randomly divided into the following four groups: A sham group, a model group, a model group treated with apocynin and a model group treated with lycopene. Immunohistochemistry and transmission electron microscopy (TEM) were used to detect the carotid structures in these groups. Quantitative polymerase chain reaction (qPCR) and western blot analysis were performed to detect the mRNA and protein expression levels of the proteins involved in cell proliferation and oxidative stress, including anti‑proliferating cell nuclear antigen, extracellular signal-regulated kinase, nicotinamide adenine dinucleotide phosphate oxidase 1, hydroxymethyl glutaric acyl coenzyme A reductase, adenosine triphosphate‑binding cassette transporter A1 and human neutrophil cytochrome b light chain. Immunohistochemistry and TEM indicated that lycopene treatment significantly reduced the intima/media ratios, the accumulation of lipids and the formation of foam cells in carotid plaques in rabbit restenosis models. Furthermore, lycopene regulated the blood lipid levels and suppressed the oxidative stress in these models. In addition, qPCR and western blot analyses revealed that lycopene significantly decreased the expression levels of cell proliferation‑associated proteins, as well as proteins involved in lipid synthesis and transportation. The results suggest that lycopene may regulate lipid metabolism and suppress oxidative stress, and thus, represents a promising therapeutic against neointimal hyperplasia.

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Multiscale bio-chemo-mechanical model of intimal hyperplasia

Jansen

Escriva

Godeferd

et al. 2022

Biomech Model Mechanobiol

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We consider a computational multiscale framework of a bio-chemo-mechanical model for intimal hyperplasia. With respect to existing models, we investigate the interactions between hemodynamics, cellular dynamics and biochemistry on the development of the pathology. Within the arterial wall, we propose a mathematical model consisting of kinetic differential equations for key vascular cell types, collagen and growth factors. The luminal hemodynamics is modelled with the Navier-Stokes equations. Coupling hypothesis among time and space scales are proposed to build a tractable modelling of such a complex multifactorial and multiscale pathology. A one-dimensional numerical test-case is presented for validation by comparing the results of the framework with experiments at short and long timescales. Our model permits to capture many cellular phenomena which have a central role in the physiopathology of intimal hyperplasia. Results are quantitatively and qualitatively consistent with experimental findings at both short and long timescales.

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Neointimal Hyperplasia: Basic Considerations

Cited by 4 publications

References 142 publications

Patient-Specific, Multi-Scale Modeling of Neointimal Hyperplasia in Vein Grafts

Patient-Specific, Multi-Scale Modeling of Neointimal Hyperplasia in Vein Grafts

Lycopene inhibits neointimal hyperplasia through regulating lipid metabolism and suppressing oxidative stress

Multiscale bio-chemo-mechanical model of intimal hyperplasia

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