1. INTRODUCTION PE is a major contributor to maternal and fetal/neonatal mortality and morbidity, affecting about 5% - 8% of pregnancy, but occurring up to 10% in China. In the mother, it can cause multi-system dysfunction including renal failure, hepatic failure, coagulopathy and central nervous system disorders. To the fetus, it may lead to fetal growth restriction, prematurity and perinatal death. However, an increasing number of women are involved in this severe complication. Currently, inadequate an- tenatal care has given to the pregnant women. There is a need for a widely applicable screening test that could permit early prediction and diagnosis of PE. Attention has turned towards identifying non-invasive, blood-borne or urinary maternal biomarkers that could predict the development and help to the monitoring of this severe complication of pregnancy. Understanding of the path- ology mechanism for PE would enable a better con- duction for this task [1-3]. Although the precise origin of PE remains unclear, the changes of placenta have been confirmed to play a middle role in pathology alternations of PE. Inadequate invasion of placental trophblast could be responsible for the origin of the disease. In normal conditions, the inva-
sion of trophblast causes the replacement of the muscular and elastic layers of the spiral arteries by fibrous tissue and then establishes a low-resistance fetoplacental blood supply. In PE, there could be an impaired tissue and arterial invasion by trophoblast cells, which may result in an unsuccessful transformation of spiral arteries and increased placental ischemia and necrosis. It has been reported that placenta ischemia may lead to an extra release of circulation toxin that might cause the patho- physiology alternations in PE [1,3-5]. To date, some factors have been reported to be related to the pathology changes of the disease, some of which have been regarded to be candidate markers of PE. We here present an overlook of some pathogenic factors correlated with placenta pathology changes in PE, which we hope could do a little conduction to the later re- searches in the future.
1. INTRODUCTION PE is a major contributor to maternal and fetal/neonatal mortality and morbidity, affecting about 5% - 8% of pregnancy, but occurring up to 10% in China. In the mother, it can cause multi-system dysfunction including renal failure, hepatic failure, coagulopathy and central nervous system disorders. To the fetus, it may lead to fetal growth restriction, prematurity and perinatal death. However, an increasing number of women are involved in this severe complication. Currently, inadequate an- tenatal care has given to the pregnant women. There is a need for a widely applicable screening test that could permit early prediction and diagnosis of PE. Attention has turned towards identifying non-invasive, blood-borne or urinary maternal biomarkers that could predict the development and help to the monitoring of this severe complication of pregnancy. Understanding of the path- ology mechanism for PE would enable a better con- duction for this task [1-3]. Although the precise origin of PE remains unclear, the changes of placenta have been confirmed to play a middle role in pathology alternations of PE. Inadequate invasion of placental trophblast could be responsible for the origin of the disease. In normal conditions, the inva- sion of trophblast causes the replacement of the muscular and elastic layers of the spiral arteries by fibrous tissue and then establishes a low-resistance fetoplacental blood supply. In PE, there could be an impaired tissue and arterial invasion by trophoblast cells, which may result in an unsuccessful transformation of spiral arteries and increased placental ischemia and necrosis. It has been reported that placenta ischemia may lead to an extra release of circulation toxin that might cause the patho- physiology alternations in PE [1,3-5]. To date, some factors have been reported to be related to the pathology changes of the disease, some of which have been regarded to be candidate markers of PE. We here present an overlook of some pathogenic factors correlated with placenta pathology changes in PE, which we hope could do a little conduction to the later re- searches in the future.
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