Fig. 4.

The immune dysregulation hypothesis elucidating the pathogenesis of PE.

Abnormal cytokine release in PE patients increases CRP and NGAL expression, leading to placental or renal damage. Placenta-derived factors induce the activation of neutrophils, which in turn produce more inflammatory cytokines to activate the immune response and promote the development of PE. In addition, the activation of neutrophils will also generate a large number of Nets. The dashed line in the figure indicates that this biomarker still needs to be verified by more large-scale clinical longitudinal studies as an indicator to predict the risk of PE.