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- N. V. Prokazova
- Institute of Experimental Cardiology, Russian Cardiology Research Center Academy of Medical Sciences Moscow Russia
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- L. D. Bergelson
- Institute of Experimental Cardiology, Russian Cardiology Research Center Academy of Medical Sciences Moscow Russia
抄録
<jats:title>Abstract</jats:title><jats:p>The ganglioside levels in atherosclerotic lesions of human aorta are considerably higher than those in unaffected areas of aorta, and atherosclerotic patients frequently have increased concentrations of serum gangliosides. The present review summarizes recent findings that suggest the possible involvement of aortic gangliosides in platelet activation and adhesion of platelets to the vessel wall. The effect of gangliosides on the structure of low density lipoproteins (LDL), on the interaction of LDL with macrophages and hepatic cells and on the LDL‐regulated biosynthesis of cholesterol is also discussed.<jats:italic>In vitro</jats:italic> experiments have demonstrated that a major ganglioside of the intima of atherosclerotic aorta induces rapid adhesion, aggregation and spreading of platelets. Moreover, gangliosides present in elevated amounts in the intercellular space of atherosclerotic aortic tissue modify the surface structure and stimulate aggregation of LDL. Ganglioside‐modified LDL are readily recognized and taken up by macrophages, while preincubation of LDL with low concentrations of gangliosides inhibits LDL binding to hepatic cells. Thus, ganglioside enrichment of LDL is likely to interfere with LDL clearance<jats:italic>via</jats:italic> the hepatic cells. Thus, ganglioside enrichment of LDL is likely to interfere with LDL clearance<jats:italic>via</jats:italic> the hepatic LDL receptor, and to stimulate binding of LDL to the scavenger receptor of macrophages. It is postulated that high ganglioside levels in the aorta and serum may be an additional risk factor in atherosclerosis.</jats:p>
収録刊行物
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- Lipids
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Lipids 29 (1), 1-5, 1994-01
Wiley
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詳細情報 詳細情報について
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- CRID
- 1362825895050799616
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- NII論文ID
- 30022608235
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- ISSN
- 15589307
- 00244201
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- データソース種別
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