Oxidized modifications of LDL (oxLDL) are known to play a major role in endothelial dysfunction and the development of atherosclerosis. In this study, we provide comparative analysis of the effects of two major types of oxLDL, copper oxidized LDL (Cu²⁺-oxLDL) and Lipoxygenase oxidized LDL (LPO-oxLDL) on proliferation of Human Aortic Endothelial Cells (HAECs). We show that Cu²⁺-oxLDL enhances HAECs proliferation in a dose and oxidation-dependent manner. Similarly, LPO-oxLDL also has a positive effect on HAECs proliferation. Mechanistically, both Cu²⁺-oxLDL and LPO-oxLDL enhance HAECs proliferation via the same pathway: Rho activation, Akt phosphorylation and a decrease in the expression of Cyclin-dependent kinase inhibitor 1B (p27^kip1). Specifically, both, Cu²⁺-oxLDL or LPO-oxLDL significantly increase Akt phosphorylation whereas inhibiting Akt with a specific inhibitor MK2206 blocks oxLDL-induced increase in the proliferation of HAECs. Furthermore, blocking Rho with C3 or its downstream target ROCK with Y27632 significantly inhibits oxLDL-induced Akt phosphorylation and cell proliferation induced by both Cu²⁺- and LPO-oxLDL. In contrast, blocking Rac1 with NSC23766 inhibitor has no effect neither on oxLDL-induced Akt phosphorylation or cell proliferation of HAECs. Further evidence shows that oxLDL-induced Rho/Akt pathway leads to downregulation of p27^kip1, a well-known negative regulator of cell proliferation. Notably, we also show that preloading cells with cholesterol prevents oxLDL-induced Akt phosphorylation and its proliferative effect. These observations contribute to our understanding of oxLDL-induced proliferative effect in endothelial cells and provide new evidence for the differential effects of oxLDL and cholesterol on endothelial function.