Interactions Between Lipoproteins and PGI2 Under Physiologic and Pathophysiologic Conditions
Nordøy et al. (1) have proved that LDL inhibit generation of an antiplatelet principle by cultured arterial endothelial cells and suggested it to be a PGI2-like substance. Starting out from these results we have been carring out systematic studies (2–8) to assess our working hypothesis that interactions between lipoproteins (LP) and prostacyclin (PGI2) could be relevant to the pathogenesis of atherosclerosis.
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