Fig. 3.

The oxidative stress hypothesis explaining the pathogenesis of PE.

Elevated Hcy level in PE patients may lead to endothelial damage and systemic inflammation through a variety of pathways, and participate in the pathogenesis of PE. Moreover, Hcy also promotes the rise of ROS levels, induces the apoptosis of trophoblast cells, and destroys the placental barrier, which increases the level of HbF in maternal peripheral blood and further exacerbates oxidative stress. To resist the damage caused by oxidative stress, the liver or lymphocytes release more A1M to clear free oxygen radicals from the body. The dashed lines in the figure indicate that these biomarkers still need to be verified by more large-scale clinical longitudinal studies as indicators to predict the risk of PE.