Abstract
The concept of elevated serum cholesterol level as a principal risk factor in the etiology of atherosclerotic lesions has evolved from several large-scale epidemiological studies (1,2,3). These studies clearly link increased serum low-density lipoprotein (LDL) levels to mortality due to myocardial infarction. LDL is a cholesterol-rich, apo B100 containing particle which has been implicated in the forward transport of cholesterol to peripheral cells, including the smooth muscle cells of the arterial wall, by way of the classical LDL receptor (4). While the role of this particle, and its ligand (apo B100)-receptor complex, in the central hepatic metabolism of cholesterol has been well studied, little is known of the mechanism by which elevated LDL levels initiate and maintain lesion development and progression in the arterial wall.
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Tulenko, T.N., Mason, R.P., Chen, M., Tasaki, H., Rock, D., Stepp, D. (1993). Atherogenic Activity caused by Excess Membrane Cholesterol in Arterial Smooth Muscle: Role of Calcium Channels. In: Godfraind, T., Paoletti, R., Govoni, S., Vanhoutte, P.M. (eds) Calcium Antagonists. Medical Science Symposia Series, vol 3. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-1725-8_16
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DOI: https://doi.org/10.1007/978-94-011-1725-8_16
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