Abstract
Preeclampsia (PE) refers to a group of dysfunction syndromes associated with elevated blood pressure and proteinuria in women with previously normal blood pressure after 20 weeks of pregnancy, and it may be accompanied by symptoms including headache, vertigo, nausea and vomiting, and epigastric discomfort (Steegers et al., 2010). It is affected by a variety of risk factors and follows a distinctive disease progression, although its pathogenesis is still unknown. Upon termination of a PE pregnancy, the clinical symptoms of PE improve rapidly, suggesting that PE is a disease originating in the placenta. Recent studies have shown that excessive apoptosis of trophoblast cells and reduced trophoblast infiltration capacity can lead to superficial implantation of the placenta, a lack of spiral arteriole remodeling, and insufficient placental perfusion leading to placental ischemia and hypoxia, all of which are important factors that cause the onset of PE (Eddy et al., 2019). Therefore, there appears to be a close relationship between excessive trophoblast cell apoptosis and development of PE. Recently, increasing evidence has shown that in patients with PE, endoplasmic reticulum (ER) stress can cause trophoblast cell apoptosis, and this finding has become an important feature of the placental pathology of PE (Lorenzon-Ojea et al., 2020).