Preeclampsia (PE) remains a leading cause of maternal and perinatal morbidity and mortality in obstetrics worldwide. No effective treatments to reduce its incidence and severity in clinical practice are currently available. A variety of hypotheses have been generated aiming to explain the origins of PE, notably being the genetic predispositions and placental dysfunction. As regard to placental dysfunction, much progress has been made in basic research and several potential therapeutic targets have been identified. This review will discuss in detail the potential therapeutic targets in PE models including uteroplacental blood flow, oxidative stress, vasoactive factors and inflammation/immune response, and introduce the evolving technologies for placental research nowadays.