Considering that oxidized low-density lipoprotein (ox-LDL) may inhibit endothelial cell (EC) migration and proliferation during endothelialization, we hypothesize that the Id1 protein promotes endothelialization exposed to ox-LDL. Cell proliferation was evaluated by cell counts, and cell migration was evaluated by wound closure assay. The role of Id1 in the cell migration and proliferation was appraised through building Id1 overexpression and silencing ECs. Here, we report that Id1 in human umbilical vascular ECs (HUVECs) was up-regulated by ox-LDL in a dose- and time-dependent manner. Low concentrations of ox-LDL increased the proliferation and migration of EC. High concentrations of ox-LDL suppressed HUVECs proliferation and migration, whose inhibitory effects were abolished by Id1 over-expression. Attenuated proliferation and migration of ECs exposed to high concentrations of ox-LDL may be correlated with the nuclear localization of p53, which was obviously weakened by over-expression of Id1 and strengthened by silencing Id1. Collectively, changes in EC, comprising proliferation and migration, upon exposure to various concentrations of ox-LDL are, at least in part, attributed to the modulatory effect of the Id1 protein, which suggests that manipulating Id1 protein activity may offer therapeutic opportunities to promote re-endothelialization under high concentrations of ox-LDL.