作者: Oguogho A , Leitinger N , Rodrigues M , Sinzinger H
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摘要: Beside prostaglandin (PG) I2 and tissue plasminogen activator (tPA), nitric oxide (NO) is a key fepellant substance contributing to haemostatic balancing. The role of low-density lipoproteins (LDL) in the pathogenesis atherosclerosis has been gaining increasing importance. It well accepted that LDL their modified (i.e. oxidized) form are no longer recognized by LDL-receptor, but taken up cells arterial wall, especially macrophages, non-regulated manner through so called scavenger-receptor pathway. This process leads formation foam cells, hallmark atherosclerotic lesion. NO also produced relevant amounts macrophages. interaction with macrophages thus importance onset early lesions. While oxidized (oxLDL) resulting decreased availability, seems prevent LDL-oxidation. In contrast, however, presence superoxides oxidation may result. All these potential actions have be discussed view extremely short half-life indicating restricted most likely local site biosynthesis being dependent on actual concentration, duration availability transition metals. These findings indicate play dual pro- antiatherosclerotic factors only.