Preeclampsia (PE) is a pregnancy-associated disease characterized by hypertension and proteinuria, and the leading cause of maternal and fetal mortality worldwide. PE is believed to be caused by alterations in feto-maternal communication. Since extracellular vesicles (EV) are crucial for cell-to-cell communication, their role in pregnancy and pregnancy-associated diseases has been a matter of active investigation. Recent evidence points to the role of maternal and placental EV in the regulation of angiogenesis, hormonal and immune mechanisms during pregnancy. This minireview focuses on how alterations in the levels of maternal and fetal EV may contribute to the pathogenesis of preeclampsia. A better understanding of fetomaternal EV crosstalk with cellular and molecular signaling pathways involved in fetal development may be crucial to early diagnosis and therapeutic interventions for PE.