Retraction: Etiopathology of preeclampsia — Recent progress from the perspective of a poor/ischemic placenta

Abstract

Research on the etiopathology of preeclampsia has rapidly progressed since the mid-20th century. However, the pathogenesis of this disease remains poorly understood. The etiology of preeclampsia may begin from poor placentation in early gestation, which can lead to placental ischemia / hypoxia. Placental hypoxia induces antiangiogenesis, angiotensin II type 1 receptor agonistic antibodies, and cytokines, resulting in vasculoendothelial dysfunction. This reduces the production of nitric oxide and increases the secretion of endothelin-1. In addition, maternal constitutional factors, such as environmental, genetic, and immunological factors, as well as oxidative stress and inflammation, are likely to contribute to the pathogenesis of abnormal placentation and maternal sensitivity to antiangiogenic factors. Therefore, early-onset preeclampsia is considered more of a placental disease. On the other hand, late-onset preeclampsia results from an imbalance of placental blood supply and fetal demand when the uterine capacity approaches its limit. Accordingly, late-onset preeclampsia is considered more of a maternal disease.