Abstract
Preeclampsia (PE), a pregnancy-specific disorder, is characterized by maternal hypertension and proteinuria or another accompanying sign/symptom of multiorgan dysfunction. Maternal symptoms resolve with delivery of the baby and, importantly, the placenta. Therefore, the placenta plays a causal role in PE. However, the precise cause of abnormal placental development and/or function is unknown. Women with obesity have an increased risk of developing PE that is potentially related to the increased inflammation that accompanies increased maternal adiposity. Furthermore, inflammatory adipokines, i.e., leptin, have been linked to the development of systemic inflammation, hypertension, and other adverse outcomes associated with PE. Rodent models that recapitulate key pathophysiological features of the maternal and fetal syndrome have been used translationally to study PE. This review covers inflammatory adipokines, immune cells, and impaired placental development associated with PE in women and in rodent models of PE that use functional genomics to test causation.