Recent insights into the pathophysiology of preeclampsia

Abstract

Preeclampsia, characterized by new-onset gestational hypertension and proteinuria, is a common and serious complication of pregnancy. Evidence from both animal and human studies has implicated placental ischemia and hypoxia as a central causative factor in the etiology of the disorder. The ischemic placenta in turn initiates a cascade of secondary effector mechanisms, including altered proangiogenic and antiangiogenic factor balance, increase in maternal oxidative stress and endothelial and immunological dysfunction. The full elucidation of these mechanisms will hopefully lead to a more complete understanding of the etiology of preeclampsia and lead to successful therapeutic intervention through the targeted disruption of new and novel pathways.

Figure 1. Placental ischemia initiates numerous pathways in the pathophysiology of preeclampsia

AT1-AA: Angiotensin 1 receptor autoantibody; ET-1: Endothelin-1; HIF-1α: Hypoxia-inducible factor-1α; NO: Nitric oxide; ROS: Reactive oxygen species; sEng: Soluble endoglin; sFlt-1: Soluble fms-like tyrosine kinase-1.