Fig. 8.
Summary of the proposed signaling events for oxLDL-induced endothelial proliferative response. Briefly, we propose that the products of LDL oxidation, such as oxidized phospholipids and oxysterols, disrupt the lipid bilayer of the membrane, which results in the activation of RhoA/ROCK cascade, possibly via dissociation of the GDI-RhoA complex, and leads to the activation of Akt1, which is known to induce cell proliferation via a decrease in the expression of cyclin-dependent kinase inhibitor 1B (p27kip1). HETE, hydroxyeicosatetraenoic acid; POVPC, 1-palmitoyl-2-(5′-oxo-valeroyl)-sn-glycero-3-phosphocholine; PGPC, 1-palmitoyl-2-glutaryl-sn-glycero-3-phosphocholine.