Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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.

Original publication




Journal article


Cardiovasc Res

Publication Date





284 - 293


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