Figure 1. Remnant lipoprotein uptake is mediated by LDLR, HSPGs, and LRP.

HSPGs are abundant in the matrix of the space of Disse and on the surface of hepatocytes. Sulfate groups (SO₄) on HSPGs interact with apoE, LPL, and HL. ApoE and possibly LPL and HL serve as ligands mediating sequestration, binding, and uptake of the remnants. Defective apoE, which occurs in type III HLP, displays variable defective binding to the LDLR and HSPGs compared with normal apoE. The LDLR, HSPGs, and the HSPG/LRP complex serve as receptors or coreceptors mediating remnant lipoprotein uptake (i–iii). E, apoE. Modified from the Journal of Lipid Research (1).