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Thin-cap fibroatheromas (TCFAs) or vulnerable atherosclerotic plaques are considered a high-risk phenotype for acute cardiovascular events. TCFAs are identified by a thin rupture-prone fibrous cap, a large necrotic core, and a high content of leucocytes. Atherogenesis is dependent upon complex patterns of blood flow. Slow-flowing blood imposing low shear stress on the arterial wall up-regulates inflammatory signalling in endothelial cells and leucocytes, and modulates microRNAs to promote inflammation and monocyte recruitment. Hence, low shear stress is believed to promote conditions conducive to vulnerable plaque development. In this review, we explore how biomechanical factors modulate macrophage phenotype and plaque stability.

Type

Journal article

Journal

Cardiovascular research

Publication Date

07/2013

Volume

99

Pages

284 - 293

Addresses

Kennedy Institute of Rheumatology, Imperial College London and University of Oxford, 65 Aspenlea Road, London W6 8LH, UK.

Keywords

Macrophages, Animals, Humans, Rupture, Spontaneous, Fibrosis, Necrosis, MicroRNAs, Mechanotransduction, Cellular, Macrophage Activation, Regional Blood Flow, Phenotype, Stress, Mechanical, Atherosclerosis, Hemodynamics, Plaque, Atherosclerotic, Biomechanical Phenomena