Figure 1.

Illustration of putative differences in the underlying etiology of ePE versus lPE. The primary lesion in deep placentation plays a leading role in the development of ePE. Failure of spiral artery modification may involve aberrant maternal inflammation due to reduced PP13 expression. By leading to placental insufficiency, this results in the liberation of inflammatory trophoblast micro-debris and imbalance in pro- and anti-angiogenic factors, events which precede clinical symptoms. In lPE, the placental lesion is insufficient to trigger development of clinical symptoms, bur rather renders the maternal system highly susceptible to secondary signals, such as obesity, which then initiate the etiological cascade leading to onset of symptoms.

ePE: Early preeclampsia; lPE: Late preeclampsia.