Uterine spiral artery (SpA) remodeling is critical for a successful pregnancy. The deficiency of SpA remodeling seriously affects the blood perfusion of the placenta, impacting the nutritional supply to the fetus and therefore fetal growth and development, which is one of the pathological causes of pregnancy related diseases. This process involves the interaction between all cells and related factors at the maternal-fetal interface, especially extravillous trophoblast cells (EVT), vascular smooth muscle cells (VSMCs) and decidual immune cells. Osteopontin (OPN), as a glycosylated protein, is widely localized in the extracellular matrix and participates in a variety of cellular activities such as migration, adhesion, differentiation and survival. OPN plays an important role in placental development, uterine decidualization and pregnancy success. This study focuses on the role of OPN in uterine spiral artery remodeling and its related molecular mechanism.