Abstract
The fundamental cellular and biochemical processes that occur in human and experimental atherosclerosis are proliferation of smooth muscle cells, accumulation of intra- and extracellular lipids, and deposition of such intercellular ground substances as collagen, elastin and proteoglycans (Ross and Glomset 1973). Of these changes, we focus our attention on the arterial wall lipids, since they are of particular importance in initiation and development of atherosclerosis for the following seven reasons; (i) the arterial wall is a catabolic site of serum low density lipoproteins (LDL) carrying the major portion of cholesteryl esters, (ii) the derangement of catabolic process of LDL in arterial tissue leads to accumulation of lipids in situ, (iii) the arterial lipid contents are related to both the serum lipid level and the severity of lesions, (iv) in experimental animals atherosclerosis can be induced by cholesterol feeding, (v) it regresses when serum cholesterol is lowered both in man and animals, (vi) the other risk factors alone can not produce atherosclerosis without hypercholesterolemia and (vii) there is no atherosclerosis without accumulation of lipids in arterial tissues.
This work was partly supported by a grant-in-aid for scientific research (C-357312) Ministry of Education, Science and Culture, Japan (1978), and the grants-in-aid for research from Keio Health Counseling Center, Tokyo (1978).
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Hata, Y., Shigematsu, H., Aihara, K., Yamamoto, M., Yamauchi, Y., Oikawa, T. (1980). Cholesteryl Ester-Rich Lipid Inclusions in the Development of Experimental Atherosclerosis in Rabbits. In: Gotto, A.M., Smith, L.C., Allen, B. (eds) Atherosclerosis V. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-6071-4_104
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DOI: https://doi.org/10.1007/978-1-4612-6071-4_104
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