Biomechanical modeling and morphology analysis indicates plaque rupture due to mechanical failure unlikely in atherosclerosis-prone mice
Ian C. Campbell,Daiana Weiss,Jonathan D. Suever,Renu Virmani,Alessandro Veneziani,Alessandro Veneziani,Raymond P. Vito,John N. Oshinski,John N. Oshinski,W. Robert Taylor,W. Robert Taylor,W. Robert Taylor +11 more
TLDR
The results suggest that if plaque rupture is possible in mice, it may be driven by a different mechanism than mechanics, and the relative distribution of stresses in the walls of murine and human plaques is computed.Abstract:
Spontaneous plaque rupture in mouse models of atherosclerosis is controversial, although numerous studies have discussed so-called “vulnerable plaque” phenotypes in mice. We compared the morphology...read more
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Transforming Growth Factor–β Signaling in T Cells Promotes Stabilization of Atherosclerotic Plaques Through an Interleukin-17–Dependent Pathway
Anton Gisterå,Anna-Karin L. Robertson,Anna-Karin L. Robertson,John Andersson,Daniel F. J. Ketelhuth,Olga Ovchinnikova,Stefan K. Nilsson,Anna M. Lundberg,Ming O. Li,Richard A. Flavell,Göran K. Hansson +10 more
TL;DR: It is reported that transforming growth factor–β (TGF-β) promotes plaque stabilization through the effects of interleukin-17 (IL-17), and this data link IL-17A to induction of a stable plaque phenotype, could lead to new plaque-stabilizing therapies, and should prompt an evaluation of cardiovascular events in patients treated with IL- 17 receptor blockade.
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Oxidized Low‐Density Lipoprotein (OxLDL)–Treated Dendritic Cells Promote Activation of T Cells in Human Atherosclerotic Plaque and Blood, Which Is Repressed by Statins: microRNA let‐7c Is Integral to the Effect
TL;DR: In this article, the effects of statins on human dendritic cells and T-cell activation were studied, showing that atorvastatin and simvastatatin suppressed the DC maturation showing lower expression of CD80, CD83, and CD86, and limited their production of tumor necrosis factor, IL-1β and IL-6, and increased transforming growth factor β and IL10 secretion.
Journal ArticleDOI
Induction of Dendritic Cell–Mediated T-Cell Activation by Modified but Not Native Low-Density Lipoprotein in Humans and Inhibition by Annexin A5: Involvement of Heat Shock Proteins
Anquan Liu,Julia Yue Ming,Roland Fiskesund,Ewa Ninio,Sonia-Athina Karabina,Claes Bergmark,Anna G. Frostegård,Johan Frostegård +7 more
TL;DR: Modified forms of LDL such as LDLx but not native LDL activate human T cells through DCs and promotes induction of regulatory T cells and is potentially interesting as a therapeutic agent.
Journal ArticleDOI
Mouse models of plaque rupture.
TL;DR: Although no mouse model examined completely simulates the entire process of plaque rupture, the brachiocephalic artery in ApoE-deficient mice fed a high-fat diet, with or without angiotensin II infusion, is a practically feasible model for plaque rupture.
Journal ArticleDOI
Three-dimensional numerical simulation of blood flow in mouse aortic arch around atherosclerotic plaques
Pauline Assemat,James A. Armitage,James A. Armitage,James A. Armitage,Karen K. Siu,Karen K. Siu,Karla G. Contreras,Anthony M. Dart,Jaye Chin-Dusting,Kerry Hourigan +9 more
TL;DR: The purpose of the present work is to include more realistic conditions for the numerical calculations of the blood flow by implementing real geometries with plaques in the numerical model, and introduce a new hemodynamical parameter to relate the location of plaques to the characteristics of the flow in the healthy configuration.
References
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Compensatory Enlargement of Human Atherosclerotic Coronary Arteries
Seymour Glagov,Elliot Weisenberg,Christopher K. Zarins,Regina Stankunavicius,George J. Kolettis +4 more
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TL;DR: Of the three types of coronary thrombosis, a precursor lesion for acute rupture has been postulated and the non-thrombosed lesion that most resembles the acute plaque rupture is the thin cap fibroatheroma (TCFA).
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Angiotensin II promotes atherosclerotic lesions and aneurysms in apolipoprotein E–deficient mice
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Distribution of circumferential stress in ruptured and stable atherosclerotic lesions. A structural analysis with histopathological correlation.
TL;DR: Data suggest that concentrations of circumferential tensile stress in the atherosclerotic plaque may play an important role in plaque rupture and myocardial infarction, however, plaque rupture may not always occur at the region of highest stress, suggesting that local variations in plaque material properties contribute to plaque rupture.
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A constrained mixture model for growth and remodeling of soft tissues
TL;DR: It was thought that the most important characteristics of soft tissues were their complex mechanical properties: they often exhibit nonlinear, anisotropic, nearly incoherent, and often incoherent properties as discussed by the authors.