Pathogenesis of Preeclampsia

被引:521
作者
Young, Brett C. [1 ,2 ]
Levine, Richard J. [3 ]
Karumanchi, S. Ananth [1 ,2 ,4 ]
机构
[1] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA
[2] Harvard Univ, Sch Med, Boston, MA 02215 USA
[3] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA
[4] Howard Hughes Med Inst, Boston, MA 02215 USA
关键词
hypertension; pregnancy; sFltl; placenta; ischemia; ENDOTHELIAL-GROWTH-FACTOR; ELEVATED LIVER-ENZYMES; FACTOR RECEPTOR-1; TYROSINE KINASE-1; SOLUBLE ENDOGLIN; ANGIOTENSIN-II; GESTATIONAL HYPERTENSION; TROPHOBLAST DIFFERENTIATION; AGONISTIC AUTOANTIBODIES; ANTIANGIOGENIC FACTORS;
D O I
10.1146/annurev-pathol-121808-102149
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Preeclampsia is a systemic syndrome that occurs in 3 to 5% of pregnant women and classically manifests as new-onset hypertension and proteinuria after 20 weeks of gestation. Preeclampsia is a leading cause of maternal and neonatal morbidity and mortality. The only known cure is delivery of the placenta. Recent discoveries, however, have led to important advances in understanding the Pathogenesis of the condition. Placental antiangiogenic factors are upregulated and disrupt the maternal endothelium. This change in the normal angiogenic balance toward an antiangiogenic state can result in hypertension, proteinuria, glomerular endotheliosis, HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome, and cerebral edema-the clinical signs of preeclampsia and eclampsia. The regulation of these antiangiogenic factors in the placenta is unknown. The recent discoveries of upregulated antiangiogenic factors provide promise for future testing to predict and diagnose preeclampsia as well as therapeutic targets for amelioration of the clinical disease.
引用
收藏
页码:173 / 192
页数:20
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