Figure 6.

Potential therapeutic effect in PE. PE pathogenesis can be distinguished by two stages. Early defect placentation is believed to contribute to the development of PE by leading to uneven blood perfusion, hypoxia and increased oxidative stress, which potentially results from lysis of fetal RBCs. This leads to structural damage to the placenta and leakage of HbF and debris into the maternal side, where it contributes to the clinical manifestation of PE, the second stage, e.g., hypertension, vascular endothelial damage and proteinuria. A1M have shown promising results in several in vivo studies by reducing tissue injury, oxidative stress and Hb toxicity as well as reduction of hemolysis of fetal RBCs in vitro.