The human malarial parasite Plasmodium falciparumis responsible for an estimated 300-500 million clinical cases and 1-3 million deaths annually. At particular risk of developing severe, life-threatening malaria-associated complications are women during their first pregnancy. The observed pathologies, such as premature delivery, intrauterine growth retardation, abortion, and death of the mother and the newborn, are in large parts due to the parasite's ability to render infected erythrocytes adhesive and sequester in the intervillous space of infected placentas. In subsequent pregnancies, women are protected from maternal malaria through antibodies that prevent cytoadhesion of P. falciparum-infected erythrocytes in the placenta. Here, we summarize our current knowledge of the pathophysiological processes underpinning maternal malaria and discuss emerging concepts for intervention.