Atherosclerotic Lesion Size and Vulnerability Are Determined by Patterns of Fluid Shear Stress

By Caroline Cheng, D. Tempel, R. van Haperen, A. van der Baan, Frank G. Grosveld, M. Daemen, R. Krams, R. de Crom. Circulation, 2006

1,026 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Immunology, Surgery

View Paper: https://www.semanticscholar.org/paper/d7d4fe87ddc69870c9a07bc47a5c24863f79cbe0

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In Cardiology and Cardiovascular Medicine

1. J. Chiu

In Immunology

1. M. Schwartz
2. Shu Chien
3. J. Chiu

In Surgery

1. M. Schwartz
2. Shu Chien
3. J. Chiu

Citations in the corpus

• Mechanotransduction in vascular physiology and atherogenesis (2009, background): “Imposing low flow on an arterial segment was sufficient to induce atherosclerotic plaque formation in hypercholesterolaemic apolipoprotein E ( APOE )-deficient mice, which develop atherosclerosis in regions of disturbed flow that are similar to human”
• Hemodynamic shear stress and the endothelium in cardiovascular pathophysiology (2008, background): “Genetic manipulation of mice also indicates that transcriptional activity of candidate genes is linked to flow disturbances”
• Role of endothelial shear stress in the natural history of coronary atherosclerosis and vascular remodeling: molecular, cellular, and vascular behavior. (2007, background): “Low ESS indirectly prootes intimal neovascularization by inducing intimal thickning and thus ischemia, upregulating the expression of EGF (21,71) and other angiogenic factors (e.g., ngiopoietin-2) (46), enhancing local inflammation, oxidaive stress, and expression of matrix degrading enzymes and l c”
• 4D flow MRI (2012, background): “Particularly, low absolute WSS and high oscillatory shear index (OSI) are hypothesized to determine the composition of atherosclerotic lesions and the development of high-risk plaques (149,150).”
• Mechanotransduction gone awry (2009, background): “Examples for this scenario include disturbed fluid shear stress at bifurcations that trigger vascular remodelling, which can result in the development of atherosclerosi”
• Effects of Disturbed Flow on Vascular Endothelium: Pathophysiological Basis and Clinical Perspectives (2011, methodology): “In vivo observations indicate that increases or decreases in shear stress, rather than the absolute levels of shear stress, play critical roles in vascular homeostasis and remodeling (82, 281, 323, 465, 603).”
• The vascular smooth muscle cell in arterial pathology: a cell that can take on multiple roles. (2012, background): “Compared with other cathepsins, cathepsin S is characterized by its ability to be secreted, and to be active extracellularly, at neutral pH.115 In particular, cathepsin S expression is inducible in VSMCs by IL-1b,116 other cytokines, and LPS.117 On the plasma membrane, cathepsin G co-localizes with ”