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The Pivotal Role Of Lipoprotein Lipase In Atherosclerosis.

J. R. Mead, D. Ramji
Published 2002 · Medicine, Biology

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Time for primary review 33 days. Atherosclerosis, the underlying cause of heart attacks, stroke and peripheral vascular disease, is responsible for over 50% of all deaths in developed countries. The disease can generally be viewed as a form of chronic inflammation that is induced and perturbed by lipid accumulation and involves a number of components, including the damaged endothelium, monocytes/macrophages, T cells, smooth muscle cells and a regulatory network of growth factors and cytokines (see Refs. [1,2] for reviews). The process is believed to be triggered by damage to the arterial endothelial cells leading to dramatic changes in their properties and increased expression of both chemokines and adhesion molecules [1,2]. This causes an infiltration of both T lymphocytes and monocytes to the site of damage. The monocytes then differentiate into macrophages, internalise lipoproteins, and transform into lipid-loaded foam cells to form the fatty streak seen in early lesions [1,2]. This transformation of macrophages into foam cells represents a critical initial event in the pathogenesis of atherosclerosis. It is, therefore, not surprising that a major focus in cardiovascular research has been devoted to understanding the molecular basis of foam cell formation and has resulted in the identification of a key, but complex, role of the enzyme lipoprotein lipase (LPL; EC 3.1.1.34) in the process. LPL is a central enzyme in overall lipid metabolism and transport, being responsible for catalysing the hydrolysis of triglycerides transported in the bloodstream by chylomicrons and VLDL, thereby providing non-esterified fatty acids and 2-monoacylglycerols for tissue utilization [3,4]. Due to the large size of its substrates, the physiological site of LPL action is at the luminal surface of blood vessels, to which the enzyme is attached via highly charged heparan sulphate proteoglycans (HSPG) [3,4]. Mature LPL is secreted to the vascular endothelium from … * Corresponding author. Tel.: +44-29-2087-6753; fax: +44-29-2087-6753 ramji{at}cardiff.ac.uk
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