van Berkel T J, Ziere G J, Bijsterbosch M K, Kuiper J
Division of Biopharmaceutics, Leiden-Amsterdam Center for Drug Research, Sylvius Laboratories, University of Leiden, The Netherlands.
Curr Opin Lipidol. 1994 Oct;5(5):331-8. doi: 10.1097/00041433-199410000-00004.
The liver plays a decisive role in the regulation of the plasma levels of atherogenic lipoproteins. The primary liver interaction site of chylomicron remnants and VLDL remnants (beta-VLDL) is still unidentified, whereas the subsequent cellular uptake is likely to be mediated in concert by the LDL receptor-related protein and the LDL receptor. The nature of the primary interaction site of remnants (remnant receptor) might be a liver-specific proteoglycan or a liver-specific protein. Atherogenic modified LDL can be recognized by a family of scavenger receptors. A newly identified 95 kDa protein forms the most likely candidate for mediating the in-vivo uptake of oxidized LDL from the circulation and may, therefore, protect the body against the presence of oxidized LDL in the blood compartment.
肝脏在调节致动脉粥样硬化脂蛋白的血浆水平方面起着决定性作用。乳糜微粒残粒和极低密度脂蛋白残粒（β-极低密度脂蛋白）在肝脏的主要相互作用位点仍未明确，而随后的细胞摄取可能由低密度脂蛋白受体相关蛋白和低密度脂蛋白受体协同介导。残粒的主要相互作用位点（残粒受体）的性质可能是一种肝脏特异性蛋白聚糖或肝脏特异性蛋白质。致动脉粥样硬化的修饰低密度脂蛋白可被一类清道夫受体识别。一种新发现的95 kDa蛋白最有可能介导循环中氧化低密度脂蛋白的体内摄取，因此可能保护机体免受血液中氧化低密度脂蛋白的影响。
