Abstract
There is now extensive evidence suggesting that atherosclerosis begins with the formation of foam cells (the initial stage of the fatty streak) underneath an intact endothelial layer (1). An early step in foam cell formation is the adherence of monocytes to the endothelium overlying an initial accumulation of cholesterol. Subsequently, the monocytes enter the artery wall through cell gap junctions, presumably attracted by a variety of chemoattractants. Within the subendothelial space, monocytes differentiate into macrophages which may then take up lipoproteins (smooth muscle cells may also take up lipoproteins, although to a lesser extent) forming foam cells. The fatty streak, through a series of poorly defined steps, may develop into complex atherosclerotic lesions, called fibrous plaques, which may eventually lead to clinically apparent coronary artery disease (CAD). The fibrous plaques are covered by a thick cap of connective tissue and smooth muscle cells and overlay a core of necrotic cellular debris and lipid. Plaques may eventually grow large enough that they can project into the lumen of the artery, reducing blood flow. Most clinical events, such as myocardial infarctions, appear to be due to ruptures, in the margins of the fibrous plaques, which are macrophage-enriched, leading to hemorrhage into the plaque with subsequent thromboses and acute occlusion of the vessel.
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Reaven, P.D. (1994). Mechanisms of Atherosclerosis: Role of LDL Oxidation. In: Armstrong, D. (eds) Free Radicals in Diagnostic Medicine. Advances in Experimental Medicine and Biology, vol 366. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1833-4_9
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