Hayley Duckles

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Atherosclerosis is a chronic inflammatory disease of arteries that develops preferentially at branches and bends that are exposed to disturbed blood flow. Vascular function is modified by flow, in part, via the generation of mechanical forces that alter multiple physiological processes in endothelial cells. Shear stress has profound effects on vascular(More)
OBJECTIVE Although atherosclerosis is associated with systemic risk factors such as age, high cholesterol, and obesity, plaque formation occurs predominately at branches and bends that are exposed to disturbed patterns of blood flow. The molecular mechanisms that link disturbed flow-generated mechanical forces with arterial injury are uncertain. To(More)
SIGNIFICANCE Shear stress controls multiple physiological processes in endothelial cells (ECs). RECENT ADVANCES The response of ECs to shear has been studied using a range of in vitro and in vivo models. CRITICAL ISSUES This article describes some of the experimental techniques that can be used to study endothelial responses to shear stress. It includes(More)
Atherosclerosis is characterized by an accumulation of smooth muscle cells and a buildup of lipid-rich foamy macrophages within the arterial wall, which can lead to lumen narrowing and reduced blood flow or to a complete arterial blockage after plaque rupture. Atherosclerosis development is influenced by several factors, including age, sex, cholesterol(More)
Induction of the antioxidant enzyme heme oxygenase-1 (HO-1) affords cellular protection and suppresses proliferation of vascular smooth muscle cells (VSMCs) associated with a variety of pathological cardiovascular conditions including myocardial infarction and vascular injury. However, the underlying mechanisms are not fully understood. Over-expression of(More)
Blood flow generates wall shear stress (WSS) which alters endothelial cell (EC) function. Low WSS promotes vascular inflammation and atherosclerosis whereas high uniform WSS is protective. Ivabradine decreases heart rate leading to altered haemodynamics. Besides its cardio-protective effects, ivabradine protects arteries from inflammation and(More)
T-type Ca(2+) channels regulate proliferation in a number of tissue types, including vascular smooth muscle and various cancers. In such tissues, up-regulation of the inducible enzyme heme oxygenase-1 (HO-1) is often observed, and hypoxia is a key factor in its induction. HO-1 degrades heme to generate carbon monoxide (CO) along with Fe(2+) and biliverdin.(More)
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