Placental oxidative stress: from miscarriage to preeclampsia
GJ Burton, E Jauniaux - Journal of the Society for …, 2004 - journals.sagepub.com
Journal of the Society for Gynecologic Investigation, 2004•journals.sagepub.com
Objective: To review the role of oxidative stress in two common placental-related disorders
of pregnancy, miscarriage and preeclampsia. Methods: Review of published literature.
Results: Miscarriage and preeclampsia manifest at contrasting stages of pregnancy, yet both
have their roots in deficient trophoblast invasion during early gestation. Early after
implantation, endovascular trophoblast cells migrate down the lumens of spiral arteries, and
are associated with their physiological conversion into flaccid conduits. Initially these cells …
of pregnancy, miscarriage and preeclampsia. Methods: Review of published literature.
Results: Miscarriage and preeclampsia manifest at contrasting stages of pregnancy, yet both
have their roots in deficient trophoblast invasion during early gestation. Early after
implantation, endovascular trophoblast cells migrate down the lumens of spiral arteries, and
are associated with their physiological conversion into flaccid conduits. Initially these cells …
Objective: To review the role of oxidative stress in two common placental-related disorders of pregnancy, miscarriage and preeclampsia.
Methods: Review of published literature.
Results: Miscarriage and preeclampsia manifest at contrasting stages of pregnancy, yet both have their roots in deficient trophoblast invasion during early gestation. Early after implantation, endovascular trophoblast cells migrate down the lumens of spiral arteries, and are associated with their physiological conversion into flaccid conduits. Initially these cells occlude the arteries, limiting maternal blood flow into the placenta. The embryo therefore develops in a low oxygen environment, protecting differentiating cells from damaging free radicals. One embryogenesis is complete, the maternal intervillous circulation becomes fully established, and intraplacental oxygen concentration rises threefold. Onset of the circulation is normally a progressive periphery-center phenomenon, and high levels of oxidative stress in the periphery may induce formation of the chorion laeve. If trophoblast invasion is severly impaired, plugging of the spiral arteries is incomplete, and onset of the maternal intervillous circulation is premature and widespread throughout the placenta. Syncytiotrophoblastic oxidative damage is extensive, and likely a major contributory factor to miscarriage. Between these two extremes will be found differing degrees of trophoblast invasion compatible with ongoing pregnancy but resulting in deficient conversion of the spiral arteries and an ischemia-reperfusion-type pehnomenon. Placental perfusion will be impaired to a greater or lesser extent, generating commensurate placental oxidative stress that is a major contributory factor to preeclampsia.
Conclusion: Miscarriage, missed miscarriage, and early- and late-onset preeclampsia represent a spectrum of disorders secondary to deficient trophoblast invasion.
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