Examination of distinct fetal and maternal molecular pathways suggests a mechanism for the development of preeclampsia.
In pregnancy, the maternal spiral arteries must widen to nourish the growing fetus. It is this critical step in placental development that is commonly defective in the pathology of preeclampsia. Other features often observed in the placental pathology of preeclampsia include fewer invasive trophoblasts, shallow trophoblast invasion and placental thrombosis and atherotic-like changes. In this review, we propose that there are two distinct pathways, maternal and fetal, which converge on narrow spiral arteries. The unmodified (along the fetal pathway) or blocked (along the maternal pathway) spiral artery, or a combination of the two, may in turn lead to placental insufficiency and induce the maternal cascade of events leading to preeclampsia. We suggest a paradigm for the molecular developmental events that cause preeclampsia through narrow spiral arteries and focus on early events that may cause failed remodeling or blockage of the arteries, which then lead to placental insufficiency and ultimately the hypoxic placenta associated with preeclampsia. We propose that examination of the molecular mechanisms of maternal and fetal pathways that lead to the development of preeclampsia may aid researchers to focus on new potential factors in this molecular basis and ultimately in treatment of this disease.
Goldman-Wohl
Debra S
DS
Department of Obstetrics and Gynecology, Hadassah University Hospital-Mt. Scopus, Jerusalem, Israel.
Yagel
Simcha
S
D043925:Angiogenesis Inducing Agents / Q000378:metabolism; D001158:Arteries / Q000502:physiology; D005260:Female; D005333:Fetus / Q000098:blood supply / Q000276:immunology / Q000502:physiology*; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology; D008431:Maternal-Fetal Exchange; D018919:Neovascularization, Physiologic; D010920:Placenta / Q000098:blood supply / Q000276:immunology; D010927:Placental Insufficiency / Q000209:etiology / Q000276:immunology; D011225:Pre-Eclampsia / Q000209:etiology* / Q000276:immunology; D011247:Pregnancy; D014327:Trophoblasts / Q000276:immunology* / Q000378:metabolism; D014599:Uterus / Q000098:blood supply*
D043925:Angiogenesis Inducing Agents