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Essay on Role of Inflammation in Atherosclerosis

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INTRODUCTION
Cardiovascular
disease, currently the leading cause of death and illness in the United
States, Europe and most developed countries, is fast growing to become the preeminent health problem worldwide (Murray & Lopez, 1997). Atherosclerosis is a progressive disease of the large and intermediate-sized arteries characterized by accumulation of lipids and fibrous elements which cause development of fatty lesions called atheromatous plaques on the inside surfaces of the arterial walls; and is the single most important contributor to this growing burden of cardiovascular disease.
Studies on the pathophysiology of this disease has evolved over the past three decades, and a fusion of these views has led to the concept of the
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VCAM-1 binds to counter-receptors on leukocytes found in nascent atheromas (Hansson, 2005). In models of experimental atherosclerosis, expression of
VCAM-1 has been shown to increase on endothelial cells overlying nascent atheromas before leukocytes adhere to the arterial endothelium, and also mice genetically engineered to express defective VCAM-1, have shown interrupted lesion development (Cybulsky et al, 2001). Once the blood cells have attached, chemokines produced in the underlying intima stimulate them to migrate through the interendothelial junctions and into the sub-endothelial space. Morphological studies have established that this migration of leukocytes through the endothelium occurs by diapedesis between the junctions of the endothelial cells (Hansson, 2005), and is now known to be mediated by defined spectrum of chemo-attractant cytokines capable of recruiting leukocytes into the arterial intima. The monocyte chemo-attractant protein1
(MCP-1), which is over-expressed in human and experimental atheroma, appears responsible for the direct migration of mononuclear phagocytes (monocytes) that characteristically accumulate in nascent atheroma (Gu et al, 1998). Studies using compound mutant mice lacking MCP-1 or its receptor CCR2, and susceptible to atherosclerosis owing to the absence of genes encoding apoE
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