Fig. 1

Pathophysiology of preeclampsia. Genetic factors, environmental factors and immunological factors are contributing factors to preeclampsia (PE). Genetic factors mainly include single nucleotide polymorphisms in sFlt1, mutations in corin and Titin genes, transcriptionally inert and L-3 hydroxyacyl-CoA dehydrogenase deficiency. Also, maternal hyperglycemia, diabetes, chronic hypertension, obesity and preexisting cardiovascular system may also induce the PE. Immunological factors mainly include the shift from T helper cells to Th1 phenotype, inhibition of uterine NK cells, increased HLA-C trophoblasts and elevated complement levels. These factors can lead to impaired trophoblast invasion and maternal vessel narrowing, causing placental ischemia and abnormal placentation. Then, the levels of circulating soluble fms-like tyrosine kinase 1 (sFlt1) and soluble endoglin (sEng) will increase, that reduces angiogenesis and causes systemic vascular dysfunctions such as proteinuria, liver dysfunction, headache, stroke and hypertension. (Abbreviation: BMI, body mass index; sFlt1, soluble fms-like tyrosine kinase 1; sEng, soluble endoglin; SNP, single nucleotide polymorphism; TTN, Titin)