Journal of Biomechanics

2010

DOI: 10.1016/j.jbiomech.2010.06.012

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The mechanics of atherosclerotic plaque rupture by inclusion/matrix interfacial decohesion

Chien M. Nguyen

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Atherosclerosis Is a Complex Vascular Disease With Distin1

-The Complex Causality Of Chronic Kidney Disease Calls For1

Introduction1

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Cited by 6 publications

(3 citation statements)

References 35 publications

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“…Furthermore, carotid arteries exhibited nonlinear variations of circumferential stress and tangent elastic moduli, within the normal pressure range [ 12 ], and the evolution of the buckling pressures of arteries under pulsatile pressure conditions was accurately described, using a nonlinear model of elasticity [ 13 ]. Lastly, nonlinear models were also used to study the effects of luminal stenosis (and plaque morphology) on plaque stability [ 14 ], as well as the interactions between the elastic layer (extracellular matrix (ECM) cap) and the rigid, calcified cells [ 15 ].…”

Section: Atherosclerosis Is a Complex Vascular Disease With Distinmentioning

confidence: 99%

ALUminating the Path of Atherosclerosis Progression: Chaos Theory Suggests a Role for Alu Repeats in the Development of Atherosclerotic Vascular Disease

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2018

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Atherosclerosis (ATH) and coronary artery disease (CAD) are chronic inflammatory diseases with an important genetic background; they derive from the cumulative effect of multiple common risk alleles, most of which are located in genomic noncoding regions. These complex diseases behave as nonlinear dynamical systems that show a high dependence on their initial conditions; thus, long-term predictions of disease progression are unreliable. One likely possibility is that the nonlinear nature of ATH could be dependent on nonlinear correlations in the structure of the human genome. In this review, we show how chaos theory analysis has highlighted genomic regions that have shared specific structural constraints, which could have a role in ATH progression. These regions were shown to be enriched with repetitive sequences of the Alu family, genomic parasites that have colonized the human genome, which show a particular secondary structure and are involved in the regulation of gene expression. Here, we show the impact of Alu elements on the mechanisms that regulate gene expression, especially highlighting the molecular mechanisms via which the Alu elements alter the inflammatory response. We devote special attention to their relationship with the long noncoding RNA (lncRNA); antisense noncoding RNA in the INK4 locus (ANRIL), a risk factor for ATH; their role as microRNA (miRNA) sponges; and their ability to interfere with the regulatory circuitry of the (nuclear factor kappa B) NF-κB response. We aim to characterize ATH as a nonlinear dynamic system, in which small initial alterations in the expression of a number of repetitive elements are somehow amplified to reach phenotypic significance.

“…Furthermore, carotid arteries exhibited nonlinear variations of circumferential stress and tangent elastic moduli, within the normal pressure range [ 12 ], and the evolution of the buckling pressures of arteries under pulsatile pressure conditions was accurately described, using a nonlinear model of elasticity [ 13 ]. Lastly, nonlinear models were also used to study the effects of luminal stenosis (and plaque morphology) on plaque stability [ 14 ], as well as the interactions between the elastic layer (extracellular matrix (ECM) cap) and the rigid, calcified cells [ 15 ].…”

Section: Atherosclerosis Is a Complex Vascular Disease With Distinmentioning

confidence: 99%

ALUminating the Path of Atherosclerosis Progression: Chaos Theory Suggests a Role for Alu Repeats in the Development of Atherosclerotic Vascular Disease

¹

,

²

,

2018

View full text Add to dashboard Cite

Atherosclerosis (ATH) and coronary artery disease (CAD) are chronic inflammatory diseases with an important genetic background; they derive from the cumulative effect of multiple common risk alleles, most of which are located in genomic noncoding regions. These complex diseases behave as nonlinear dynamical systems that show a high dependence on their initial conditions; thus, long-term predictions of disease progression are unreliable. One likely possibility is that the nonlinear nature of ATH could be dependent on nonlinear correlations in the structure of the human genome. In this review, we show how chaos theory analysis has highlighted genomic regions that have shared specific structural constraints, which could have a role in ATH progression. These regions were shown to be enriched with repetitive sequences of the Alu family, genomic parasites that have colonized the human genome, which show a particular secondary structure and are involved in the regulation of gene expression. Here, we show the impact of Alu elements on the mechanisms that regulate gene expression, especially highlighting the molecular mechanisms via which the Alu elements alter the inflammatory response. We devote special attention to their relationship with the long noncoding RNA (lncRNA); antisense noncoding RNA in the INK4 locus (ANRIL), a risk factor for ATH; their role as microRNA (miRNA) sponges; and their ability to interfere with the regulatory circuitry of the (nuclear factor kappa B) NF-κB response. We aim to characterize ATH as a nonlinear dynamic system, in which small initial alterations in the expression of a number of repetitive elements are somehow amplified to reach phenotypic significance.

“…Furthermore, carotid arteries exhibit nonlinear variations of circumferential stress and tangent elastic moduli within the normal pressure range [6], and the evolution of buckling pressures of arteries under pulsatile pressure conditions could be accurately described by a non-linear model of elasticity [7]. Lastly, non-linear models have been also used to study the effects of luminal stenosis (and the plaque morphology) on plaque stability [8] or the interaction between the elastic layer (ECM cap) and the rigid calcified cells [9].…”

Section: -The Complex Causality Of Chronic Kidney Disease Calls Formentioning

confidence: 99%

ALUminating the Path of Atherosclerosis Progression: Chaos Theory Suggests a Role for Alu Repeats in the Development of Atherosclerotic Vascular Disease

¹

,

²

,

2018

Preprint

View full text Add to dashboard Cite

Atherosclerosis (ATH) and Coronary Artery Disease (CAD) are chronic inflammatory diseases with an important genetic background which derive from the cumulative effect of multiple common risk alleles, most of them located in genomic non-coding regions. These complex diseases behave as non-linear dynamical systems that show a high dependence on their initial conditions, so that long-term predictions of disease progression are unreliable. One likely possibility is that the non-linear nature of ATH could be dependent on non-linear correlations in the structure of the human genome. In this review we show how Chaos theory analysis highlighted genomic regions that shared specific structural constraints that could have a role in ATH progression. These regions were shown to be enriched in repetitive sequences of the Alu family, genomic parasites which colonized the human genome, which show a particular secondary structure and have been involved in the regulation of gene expression. We also review the impact of Alu elements on the mechanisms that regulate gene expression, especially highlighting the molecular mechanisms by which the Alu elements could alter the inflammatory homeostasis. We devise especial attention to their relationship with the lncRNA ANRIL, the strongest risk factor for ATH, their role as miRNA sponges, and their ability to interfere with the regulatory circuitry of the NF-kB response. We aim to characterize ATH as a non-linear dynamic system in which small initial alterations in the expression of a number of repetitive elements are somehow amplified to reach phenotypic significance.

“…Acute coronary syndrome (ACS) is typically caused by coronary atherosclerosis [1], and, specifically, by evolution of atherosclerotic plaque [2]. The pathophysiological mechanisms of atherosclerotic plaque rupture include vasospasm, plaque rupture, platelet adhesion, aggregation, and thrombus formation [3][4][5]. Vulnerable plaques have large lipid core, thin fibrous cap, intraplaque hemorrhage, and neo-vascularization of the vasa vasorum [6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Detection of Vulnerable Atherosclerotic Plaques in Experimental Atherosclerosis with the USPIO-Enhanced MRI

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et al. 2015

Cell Biochem Biophys

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This study's goal was to assess the diagnostic value of the USPIO-(ultra-small superparamagnetic iron oxide) enhanced magnetic resonance imaging (MRI) in detection of vulnerable atherosclerotic plaques in abdominal aorta in experimental atherosclerosis. Thirty New Zealand rabbits were randomly divided into two groups, Group A and Group B. Each group comprised 15 animals which were fed with high cholesterol diet for 8 weeks and then subjected to balloon-induced endothelial injury of the abdominal aorta. After another 8 weeks, animals in Group B received adenovirus carrying p53 gene that was injected through a catheter into the aortic segments rich in plaques. Two weeks later, all rabbits were challenged with the injection of Chinese Russell's viper venom and histamine. Pre-contrast images and USPIO-enhanced MRI images were obtained after pharmacological triggering with injection of USPIO for 5 days. Blood specimens were taken for biochemical and serological tests at 0 and 18 weeks. Abdominal aorta was histologically studied. The levels of serum ICAM-1 and VCAM-1 were quantified by ELISA. Vulnerable plaques appeared as a local hypo-intense signal on the USPIO-enhanced MRI, especially on T2*-weighted sequences. The signal strength of plaques reached the peak at 96 h. Lipid levels were significantly (p < 0.05) higher in both Group A and B compared with the levels before the high cholesterol diet. The ICAM-1 and VCAM-1 levels were significantly (p < 0.05) higher in Group B compared with Group A. The USPIO-enhanced MRI efficiently identifies vulnerable plaques due to accumulation of USPIO within macrophages in abdominal aorta plaques.

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