摘要: Atherosclerotic vascular disease is the leading cause of death in industrialized society. One important risk factor for onset atherosclerosis an elevated concentration low density lipoprotein (LDL), major carrier blood cholesterol (1). It thus paradoxical that LDL often fails to exert atherogenic effects vitro. These observations led suggestion has be modified promote (2,3). Subsequent studies indicate cultured arterial cells modify (4) and mechanism involves oxidative damage (5–7). Oxidized LDL, but not native exerts a multitude potentially vitro vivo (8,9), suggesting oxidation might physiologically relevant pathway modification artery wall.
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