Preeclampsia (PE) is a life-threatening complication of pregnancy; it can affect multiple organs in the mother leading to renal failure, abnormal liver function, haemolysis, seizures, severe oedema and stroke. Despite worldwide research for many years, there is no effective “cure” for PE. The current treatment is to deliver the baby, often prematurely, to save the mother’s life. Although wide-spread and multi-organ endothelial dysfunction seems to unify PE symptoms, it is increasingly recognized that PE is not a single disease but a complex syndrome. To find treatment for PE, we need to study PE subtypes and search for subtype-specific treatments.
The field is still defining how to best subtype PE. One classification is based on the timing of disease presentation, early (<34 gestation weeks) and late (>34 weeks) onset. Early-onset PE is often associated with severe disease and intrauterine growth restriction (IUGR), and requires premature delivery. Late-onset PE is rarely linked to IUGR but can also be severe. It is also suggested that early-onset PE is primarily of placental origin, whereas late-onset PE is more related to maternal failure of adaptation to pregnancy.
This talk will focus on our recent research on a serine protease that is expressed only by the placenta and significantly up-regulated in early-onset PE. Our data strongly suggests that this protease, which is of placenta-origin but circulating in the maternal blood, disturbs maternal vascular homeostasis and contributes to the development of early-onset PE. There also appears a direct link between this protease and IUGR. Our studies indicate that this protease has potential for the development of treatment for early-onset PE.