Pathogenesis and promising non-invasive markers for preeclampsia
Obstetrics & Gynecology Science
;
: 2-7, 2013.
Article
in English
| WPRIM
| ID: wpr-17408
ABSTRACT
Preeclampsia is one of the leading causes of maternal mortality/morbidity and preterm delivery in the world, affecting 3% to 5% of pregnant women. The pathophysiology of preeclampsia likely involves both maternal and fetal/placental factors. Abnormalities in the development of placental vessels early in pregnancy may result in placental hypoperfusion, hypoxia, or ischemia. Hypoperfusion, hypoxia, and ischemia are critical components in the pathogenesis of preeclampsia because the hypoperfused placenta transfers many factors into maternal vessels that alter maternal endothelial cell function and lead to the systemic symptoms of preeclampsia. There are several hypotheses to explain the pathogenesis of preeclampsia, including altered angiogenic balance, circulating angiogenic factors (such as marinobufagenin, a bufadienolide trigger), and activation of the renin-angiotensin system. Epigenetically-modified cell-free nucleic acids that circulate in plasma and serum might be novel markers with promising non-invasive clinical applications in the diagnosis of preeclampsia.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Placenta
/
Plasma
/
Pre-Eclampsia
/
Renin-Angiotensin System
/
Bufanolides
/
Nucleic Acids
/
Pregnant Women
/
Endothelial Cells
/
Angiogenesis Inducing Agents
/
Ischemia
Type of study:
Etiology study
Limits:
Female
/
Humans
/
Pregnancy
Language:
English
Journal:
Obstetrics & Gynecology Science
Year:
2013
Type:
Article
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