Mechanopathobiology of Atherogenesis: A Review

VanEpps, J. Scott; Vorp, David A.

doi:10.1016/j.jss.2006.11.001

Cited by 43 publications

(37 citation statements)

References 182 publications

(91 reference statements)

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“…Since possible contributors to the development of atherosclerosis can be categorized as biochemical or biomechanical [73] , there have also been different mathematical models developed for different objectives.…”

Section: Overview Of Existing Resultsmentioning

confidence: 99%

“…By contrast, in regions of atherogenic flow patterns, including low flow, flow separation, flow reversal and other types of disturbed flow, endothelial cells have high rates of proliferation and death, high permeability of solutes and failure to align in the direction of flow [23] . This endothelial dysfunction can also be caused by several different sources [73] , and appears to be the initial event in atherosclerosis leading to the migration of macromolecules into the intima. The infiltration and retention of excess low-density lipoproteins(LDLs) in the intima initiate an inflammatory response in the vessel wall, and the modification of LDLs through oxidation or enzymatic attack in the intima induces endothelial cells to express adhesion receptors to attract leukocytes, especially monocytes [24] .…”

Section: Inducing Factors Of Atherosclerosismentioning

confidence: 99%

“…However, it is plaque rupture with superimposed thrombus that may turn a stable disease to a life-threatening condition and induce the blockage of a main artery, which can lead to ischaemic brain or myocardial infarctions as well as other cardiovascular diseases [15;42;52] ; on the other hand, plaque rupture can also let some material of thrombus be taken away by the blood flow, and may induce the blockage in another part of the artery, turning a local problem to a global one. Possible contributors to the development of atherosclerosis can be categorized as either biochemical or biomechanical [73] . The main biochemical processes associated with atherosclerosis start with the penetration of monocytes from the blood flow into the vessel wall.…”

Section: Introductionmentioning

confidence: 99%

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Mathematical modeling and simulation of the evolution of plaques in blood vessels

et al. 2015

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The formation of plaques is one of the main causes for the blockage of arteries. This can lead to ischaemic brain or myocardial infarctions as well as other cardiovascular diseases. Possible biochemical and biomechanical processes contribute to the development of plaque growth and rupture. The main biochemical processes are the penetration of monocytes and the accumulation of foam cells in the vessel wall, leading to the formation and growth of plaques. The biomechanical forces can be measured by observing stresses in the blood flow and the vessel wall, which may lead to the rupture of plaques.In this thesis, we formulate an appropriate model to describe the evolution of plaques. The model consists of both the interaction between the blood flow and the vessel wall, and the growth of plaques due to the penetration of monocytes from the blood flow into the vessel wall. The Navier-Stokes equations and the elastic structure equations are used to describe the dynamics of fluid (blood flow) and the mechanics of structure (vessel wall). The motion of monocytes is described by the convection-diffusion-reaction equation, coupled with an equation for the accumulation of foam cells. Finally the metric of growth is introduced to accurately determine the stress tensor, and its evolution equation is derived. The variational formulation of the model is transformed into the ALE (Arbitrary Lagrangian-Eulerian) formulation, and all the equations are rewritten in the fixed domain. Temporal discretization is achieved with finite differences and spatial discretization is based on the Galerkin finite element method. The nonlinear systems are linearized and solved by the Newton method.Based on the model and the numerical methods above, numerical simulations are performed by using the software Gascoigne. The obtained numerical results make an agreement with the observation, and support the assumption that the penetration of monocytes and the accumulation of foam cells lead to the formation and growth of plaques, and that the evolution of plaques induces the increase of stresses in the vessel wall, which is an indicator of plaque rupture. Zusammenfassung

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Section: Overview Of Existing Resultsmentioning

confidence: 99%

Section: Inducing Factors Of Atherosclerosismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mathematical modeling and simulation of the evolution of plaques in blood vessels

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“…33 Em contato com o fluxo sanguíneo, as células endoteliais encontram-se expostas à tensão de cisalhamento (shear stress), gerada pela orientação do fluxo, e à tensão circunferencial secundária à distensão da parede pela pressão arterial. 18 Uma característica comum a toda célula endotelial, sem importar a localização, é a capacidade de responder a alterações nas condições hemodinâmicas, particularmente às mudanças na tensão de cisalhamento (shear stress), que atua diretamente na sua superfície, 14,15,18,23,31 originando respostas que transformam a morfologia e a função celular por meio de mudanças na expressão gênica.…”

Section: Introductionunclassified

“…14,15 Consequentemente, o papel que as tensões hemodinâmicas desempenham na regulação da função endotelial é hoje um intenso campo de pesquisa. 14,20,33,31 Fenômenos como a angiogênese e o remodelamento da parede arterial têm recebido atenção crescente com o intuito de correlacionar fatores estruturais e hemodinâmicos na formação de lesões vasculares aneurismá-ticas e aterosclerose intracraniana. 14,18,20,23,27,34,35 Essas lesões ocorrem, principalmente, em localizações de geometria complexa da árvore arterial (bifurcações e curvas arteriais), onde incidem as maiores variações espaço-temporais da tensão de cisalhamento, fluxos secundários, separação do fluxo etc.…”

Section: Introductionunclassified

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2009

Arq Bras Neurocir

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3D collagen cultures under well‐defined dynamic strain: A novel strain device with a porous elastomeric support

Tomei

Boschetti

Gervaso

2009

Biotech & Bioengineering

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The field of mechanobiology has grown tremendously in the past few decades, and it is now well accepted that dynamic stresses and strains can impact cell and tissue organization, cell-cell and cell-matrix communication, matrix remodeling, cell proliferation and apoptosis, cell migration, and many other cell behaviors in both physiological and pathophysiological situations. Natural reconstituted matrices like collagen and fibrin are often used for three-dimensional (3D) mechanobiology studies because they naturally form fibrous architectures and are rich in cell adhesion sites; however, they are physically weak and typically contain >99% water, making it difficult to apply dynamic stresses to them in a truly 3D context. Here we present a composite matrix and strain device that can support natural matrices within a macroporous elastic structure of polyurethane. We characterize this system both in terms of its mechanical behavior and its ability to support the growth and in vivo-like behaviors of primary human lung fibroblasts cultured in collagen. The porous polyurethane was created with highly interconnected pores in the hundreds of mm size scale, so that while it did not affect cell behavior in the collagen gel within the pores, it could control the overall elastic behavior of the entire tissue culture system. In this way, a well-defined dynamic strain could be imposed on the 3D collagen and cells within the collagen for several days (with elastic recoil driven by the polyurethane) without the typical matrix contraction by fibroblasts when cultured in 3D collagen gels. We show lung fibroblastto-myofibroblast differentiation under 30%, 0.1 Hz dynamic strain to validate the model and demonstrate its usefulness for a wide range of tissue engineering applications.

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Mechanopathobiology of Atherogenesis: A Review

Cited by 43 publications

References 182 publications

Mathematical modeling and simulation of the evolution of plaques in blood vessels

Mathematical modeling and simulation of the evolution of plaques in blood vessels

Untitled

3D collagen cultures under well‐defined dynamic strain: A novel strain device with a porous elastomeric support

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