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There are three fates of APOA1 through this process: (i) holoparticle uptake of the APOA1-containing HDL populations into endothelial cells which is facilitated by scavenger receptor BI (SR-BI) in cooperation with ATP-binding cassette, subfamily G, member 1 (ABCG1) [92], (ii) direct flux of cholesterol onto the APOA1-containing HDL via ABCG1 at the endothelial surface and return to circulation, and (iii), dissociation of lipid-poor APOA1 which interacts with ABCA1 on the endothelial cell surface to either accept cholesterol directly and return to circulation or is internalized into the vascular space [93]

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