Krempler F
Wien Klin Wochenschr Suppl. 1984;151:1-12.
The mechanisms of atherogenesis are under intensive clinical and experimental investigation. It is commonly accepted that lipoproteins play a major role in atherogenesis. The results of several clinical studies suggest that lipoprotein (a) [Lp(a)] represents an independent risk factor for atherosclerosis. In order to obtain information on the physiological and pathological role of Lp(a), studies were undertaken to investigate the metabolism, removal sites, and possible atherogenic mechanisms of Lp(a). It was found that Lp(a) is not a metabolic product of other apoprotein B containing lipoproteins, but appears to be synthesized as a separate lipoprotein. The turnover parameters of Lp(a) resemble those of LDL. Binding studies of Lp(a) with cultured human fibroblasts demonstrated that Lp(a) is bound by the B-E receptor. After binding, Lp(a) is internalized and inhibits cellular cholesterol synthesis. In the presence of dextran sulfate or antibodies to the specific Lp(a) apoprotein or apoprotein B, Lp(a) is avidly taken up by macrophages. A similar mechanism might be responsible for the atherogenic effect of Lp(a).
动脉粥样硬化的发病机制正处于深入的临床和实验研究中。脂蛋白在动脉粥样硬化形成过程中起主要作用，这一点已被广泛接受。多项临床研究结果表明，脂蛋白(a)[Lp(a)]是动脉粥样硬化的一个独立危险因素。为了获取有关Lp(a)生理和病理作用的信息，人们开展了多项研究来探讨Lp(a)的代谢、清除部位以及可能的致动脉粥样硬化机制。研究发现，Lp(a)并非其他含载脂蛋白B的脂蛋白的代谢产物，而是似乎作为一种独立的脂蛋白合成。Lp(a)的周转参数与低密度脂蛋白（LDL）相似。Lp(a)与培养的人成纤维细胞的结合研究表明，Lp(a)可被B-E受体结合。结合后，Lp(a)被内化并抑制细胞胆固醇合成。在存在硫酸葡聚糖或针对特定Lp(a)载脂蛋白或载脂蛋白B的抗体的情况下，Lp(a)会被巨噬细胞大量摄取。类似的机制可能是Lp(a)致动脉粥样硬化作用的原因。
