In the human placenta, embryo-derived trophoblasts aggressively invade maternal spiral arteries and transform the arteries to low-resistance large-caliber vessels. This process, which ensures adequate placental perfusion, is called maternal vascular remodeling. Histological examination showed deposition of maternal platelets in the trophoblast aggregates formed in the spiral arteries. Several lines of evidence suggest that these platelets are activated. Soluble factors released from the activated platelets, as a whole, enhanced invasive capacity of isolated trophoblasts in vitro. These findings suggest the importance of nonhemostatic platelet function in maternal vascular remodeling. In contrast, gene knockout studies suggest that maternal platelet defects are compatible with successful pregnancy in mice. Moreover, pregnant women with severe platelet defects usually accomplish an uneventful pregnancy. Thus, promotion of endovascular trophoblast infiltration by maternal platelets might not be the only mechanism that regulates maternal vascular remodeling. The maternal vascular remodeling is an essential component of human reproduction and should be secured by several complementary mechanisms. Future studies should aim to elucidate other mechanisms that could regulate endovascular trophoblast infiltration.