© 2002 by European Society of Cardiology
Copyright © 2002, European Society of Cardiology
The pivotal role of lipoprotein lipase in atherosclerosis
Cardiff School of Biosciences, Cardiff University, Museum Avenue, P.O. Box 911, Cardiff CF10 3US, UK
* Corresponding author. Tel.: +44-29-2087-6753; fax: +44-29-2087-6753 ramji@cardiff.ac.uk
Received 21 December 2001; accepted 5 March 2002
KEYWORDS apoE, apolipoprotein E; HSPG, heparan sulphate proteoglycans; IFN-
, interferon-; LPL, lipoprotein lipase; LRP, LDL receptor-related protein; M-CSF, macrophage colony stimulating factor; TNF-
, tumour necrosis factor-
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1. Introduction |
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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
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2. Pro-atherogenic actions of LPL |
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3. Importance of LPL expression in the atherosclerotic lesion |
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4. The catalytic action of LPL induces the formation of atherogenic lipoprotein remnants |
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5. LPL acts as an atherogenic ligand |
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6. Anti-atherogenic nature of LPL |
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7. Regulation of LPL by factors implicated in atherogenesis |
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8. Concluding remarks |
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