sub>2-glycoprotein I (β₂-GPI), a main autoantigen in patients with antiphospholipid syndrome (APS), binds to the negative lipid components, such as oxidized low density lipoprotein (ox-LDL) and cardiolipin, thereby forming a stable β₂-GPI immune complex. β₂-GPI immune complexes and the immune response induced by anti-β₂-GPI immune complex antibodies significantly promote the formation of atherosclerotic plaques and vascular injury in patients with antiphospholipid syndrome. This review summarized the formation mechanism and the effects of β₂-glycoprotein I immune complex and the effect of β₂-glycoprotein I immune complex in the pathogenic process. The mechanism of β₂-GPI-DⅤ blocking the formation of β₂-GPI/ox-LDL complex was introduced, which provided possible drug targets and therapeutic ideas for cardiovascular diseases, especially atherosclerosis, caused by β₂-GPI/ox-LDL immune complex.