Key result
Arteriosclerosis forms via intimal proliferation and plasma lipid infiltration into arteries with age-related thickening.
Hypothesis-generating in animal models; leaves open translation to human arteriosclerosis mechanisms and management.
The basic process in the morphogenesis of arteriosclerosis consists of proliferation and insudation in the intima, and varied combinations of these two processes produce various types of arteriosclerotic lesions. The morphogenesis of atherosclerosis is considered to be as follows: Atheroma is formed by the infiltration of blood plasma lipids into the intima of the large and medium‐sized arteries having cellulofibrous intimal thickening, which grows with age. As the result, proliferation advances especially in the upper layer of the intima. There were two types of atheroma formation. Arteriosclerosis of the small arteries and arterioles is produced by various combinations of insudation and proliferation in the small arteries and arterioles where the intimal thickening does not occur with age, or only to a slight degree, if any. In order to elucidate the mechanism of the proliferation and insudation in the intima, animal experiments were carried out. On the basis of the experimental results, possible causes of the proliferation (cellulofibrous intimal thickening) and the insudation (blood plasma infiltration) were discussed. ACTA PATH. JAP. 18:75–82, 1968.
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Genju Ooneda (1968) studied Arteriosclerosis. The morphogenesis of arteriosclerosis involves intimal proliferation and insudation, with atheroma forming via plasma lipid infiltration into arteries with age-related cellulofibrous thickening.
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