Genetic and epigenetic factors contribute to the onset of preeclampsia

Preeclampsia (PE) is a major cause of perinatal materno-foetal morbidity and pregnancy-associated-mortality in industrialized countries. Clinically, PE associates maternal pregnancy-induced hypertension with proteinuria. PE is often considered as a two-stage disease. The first stage is a shallow cytotrophoblastic invasion which induces cycles of hypoxia-reoxygenation at the placental level. Subsequently an abnormal expression pattern occurs and is followed by the release of soluble factors and trophoblastic debris in the maternal blood flow. These stimuli trigger the second phase of the disease, the maternal syndrome. Although some molecular actors have been recently identified, mechanisms of the disease onset remains poorly understood. It seems that combinations of genetic, epigenetic and environmental factors are involved. Here, we suggest that epigenetic marks have to be considered to decipher the physiopathological process of PE. Since these marks must be established early and are traceable in the maternal blood flow, they could constitute a diagnosis tool.