The liver plays a decisive role in the regulation of the plasma levels
of atherogenic lipoproteins. The primary liver interaction site for c
hylomicron-remnants and VLDL remnants (P-VLDL) is still unidentified,
while the subsequent cellular uptake is likely to be mediated in conce
rt by the LDL receptor related protein (LRP) 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. A
therogenic modified LDL can be recognized by a family of scavenger-rec
eptors. A newly identified 95-kDa protein forms the most likely candid
ate for mediating the in vivo uptake of oxidized LDL from the circulat
ion and might thus protect the body against the presence of oxidized L
DL in the blood compartment.