Aim High lipoprotein （a） ［（Lp（a）］ level had been identified as an independent risk factor for coronary and peripheral blood disease. In this study, we investigatd the effect of Lp（a） on endothelial progenitor cells （EPC） homing to the sites of hindlimb ischemia tissues and its potential mechanisms. Methods After treatment with PBS or Lp（a） for 12 h, EPC were transplanted into the hindlimb ischemia mouse model by a tail intravenous injection. The homing and vasculogenesis of EPC were determined. On the other hand, EPC adhesion ability and related gene expression were detected in vitro. Results Lp（a） inhibited homing of EPC to the sites of ischemic tissues and weakened fuction of EPC vasculogenesis. Further, Lp（a） impaired EPC adhesion ability and down-regulated expression of P-selectin glycoprotein ligand-1 （PSGL-1） as well as CXCR4 in EPC in vitro. Conclusion Lp （a） inhibited EPC homing to the sites of hindlimb ischemic tissues possibly by lowering adhesion ability of EPC and PSGL-1, CXCR4 expression in EPC.