Vascular Smooth Muscle Cells

Majesky, Mark W.

doi:10.1161/atvbaha.116.308261

Cited by 30 publications

(21 citation statements)

References 78 publications

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“…It has been reported that senescent human SMCs are not bystanders in atherosclerotic plaque progression but are involved through a proinflammatory senescence-associated secretion of multiple cytokines and chemokines. 16 Since aging causes the phenotype of VSMCs to switch from contractile to synthetic type, 17 it may further enhance the development of atherosclerosis in the infrainguinal muscular arteries as well as in the suprainguinal elastic arteries. It is known that of the 4800 chemical compounds in cigarettes, nicotine is the major constituent.…”

Section: Discussionmentioning

confidence: 99%

Distribution Pattern of Atherosclerosis in the Abdomen and Lower Extremities and Its Association with Clinical and Hematological Factors

Park

Jung

Yoon

2021

VHRM

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Section: Discussionmentioning

confidence: 99%

Distribution Pattern of Atherosclerosis in the Abdomen and Lower Extremities and Its Association with Clinical and Hematological Factors

Park

Jung

Yoon

2021

VHRM

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“…11,63 Oxidative stress in atherosclerosis results primarily from the activity of NAD(P)H oxidases. 64 However, their role in SMCs, especially in the context of atherosclerosis, remains ambiguous.…”

Section: Smooth Muscle Cellsmentioning

confidence: 99%

“…[4][5][6] This, in addition to the accumulation of cholesterol and smooth muscle cells (SMCs) in the intima, leads to the transformation of monocytes into foam cells, which consume dead cells and lipids. [7][8][9] The atherogenic process involves multiple cell types, that is, endothelial cells (ECs), 10 SMCs, 11 immune cells, 12 and stem/progenitor cells, 13 in which levels of both intracellular and extracellular reactive oxygen and nitrogen species play a fundamental role in vascular cell homoeostasis and eventually affects the development of atherosclerosis.…”

mentioning

confidence: 99%

Reactive Oxygen Species Generation and Atherosclerosis

Nowak

Deng

Ruan

et al. 2017

ATVB

126

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“…This is a key assumption. Vascular SMCs are known to be extremely plastic and capable of demonstrating a broad range of behaviours (Owens et al, 2004;Majesky, 2016), but we will consider only this particular phenotype.…”

Section: Model Descriptionmentioning

confidence: 99%

A two-phase model of early fibrous cap formation in atherosclerosis

Watson

Byrne

Macaskill

et al. 2018

Journal of Theoretical Biology

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Atherosclerotic plaque growth is characterised by chronic, non-resolving inflammation that promotes the accumulation of cellular debris and extracellular fat in the inner artery wall. This material is highly thrombogenic, and plaque rupture can lead to the formation of blood clots that occlude major arteries and cause myocardial infarction or stroke. In advanced plaques, vascular smooth muscle cells (SMCs) are recruited from deeper in the artery wall to synthesise a cap of fibrous tissue that stabilises the plaque and sequesters the thrombogenic plaque content from the bloodstream. The fibrous cap provides crucial protection against the clinical consequences of atherosclerosis, but the mechanisms of cap formation are poorly understood. In particular, it is unclear why certain plaques become stable and robust while others become fragile and dangerously vulnerable to rupture. We develop a multiphase model with non-standard boundary conditions to investigate early fibrous cap formation in the atherosclerotic plaque. The model is parameterised using data from a range of in vitro and in vivo studies, and includes highly nonlinear mechanisms of SMC proliferation and migration in response to an endothelium-derived chemical signal. We demonstrate that the model SMC population naturally evolves towards a steady-state, and predict a rate of cap formation and a final plaque SMC content consistent with experimental observations in mice. Parameter sensitivity simulations show that SMC proliferation makes a limited contribution to cap formation, and demonstrate that stable cap formation relies primarily on a critical balance between the rates of SMC recruitment to the plaque, chemotactic SMC migration within the plaque and SMC loss by apoptosis or phenotype change. This model represents the first detailed in silico study of fibrous cap formation in atherosclerosis, and establishes a multiphase modelling framework that can be readily extended to investigate many other aspects of plaque development.

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Vascular Smooth Muscle Cells

Cited by 30 publications

References 78 publications

Distribution Pattern of Atherosclerosis in the Abdomen and Lower Extremities and Its Association with Clinical and Hematological Factors

Distribution Pattern of Atherosclerosis in the Abdomen and Lower Extremities and Its Association with Clinical and Hematological Factors

Reactive Oxygen Species Generation and Atherosclerosis

A two-phase model of early fibrous cap formation in atherosclerosis

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