ACKR2 and preeclampsia: In conclusion, syncytiotrophoblast stress and cytoskeleton impairment may occur at various times during both early and late preeclampsia, leading to impairment of the cell cytoskeleton, ACKR2-mediated chemokine degradation, and ACKR2 receptor recycling, resulting in inadequate regulation of the inflammatory environment at the maternal–fetal interface (45).