The placental circulation is a dynamic network of blood vessels and during pregnancy the placental circulation must develop and remodel to accommodate the needs of the growing fetus. Therefore, placental angiogenesis is carefully regulated by having a balance between pro-angiogenic and anti-angiogenic factors. In early pregnancy, trophoblasts invade the placenta, leading to remodeling of the spiral arteries, which allows blood to flow freely to the fetus. In preeclampsia (PE), the cytotrophoblastic invasion of the spiral arteries is impaired, causing the spiral arteries to remain narrow and restricting the blood supply to the fetus. As pregnancy progresses, the effects of the restricted blood supply become more significant since the placenta is unable to keep up with the increased amount of blood and nutrients necessary for fetal development. The impaired blood and nutrient supply is believed to lead to placental ischemia, which can lead to the release of various placental factors and angiogenic factors (factors causing angiogenesis). This impairment is believed to produce the widespread endothelial dysfunction observed in PE.
Research has shown that endothelial dysfunction produces an imbalance of pro- and anti-angiogenic factors, thus, making factors involved with the angiogenesis process of placental formation and implantation good candidates as biomarkers for preeclampsia. Several circulating angiogenic factors (pro- and anti-angiogenic) have been identified and studied for their potential use as biomarkers of PE. These potential biomarkers are identified in the tables on the following two pages.
