Genetic factors, maternal factors and immunological factors may cause placental dysfunction (stage I), which in turn leads to the release of antiangiogenic factors (such as soluble fms-like tyrosine kinase 1 (sFLT1) and soluble endoglin (sENG)) and other inflammatory mediators that induce preeclampsia (stage II). AT1, angiotensin II type I receptor; dNK, decidual natural killer; ER, endoplasmic reticulum; HELLP, haemolysis, elevated liver enzymes and low platelet count; PlGF, placental growth factor; SNP, single-nucleotide polymorphism; Treg, regulatory T cell; VEGF, vascular endothelial growth factor.