Uteroplacental vascular development and placental function: an update

被引:147
作者
Reynolds, Lawrence P. [1 ]
Borowicz, Pawel P.
Caton, Joel S.
Vonnahme, Kimberly A.
Luther, Justin S.
Buchanan, David S.
Hafez, Shireen A.
Grazul-Bilska, Anna T.
Redmer, Dale A.
机构
[1] N Dakota State Univ, Ctr Nutr & Pregnancy, Fargo, ND 58108 USA
基金
美国国家卫生研究院; 美国国家科学基金会;
关键词
placenta; angiogenesis; pregnancy; fetal growth; regulation; therapeutic; ENDOTHELIAL GROWTH-FACTOR; HUMAN FETOPLACENTAL VASCULOGENESIS; SILDENAFIL CITRATE VIAGRA; FETAL-GROWTH; FACTOR EXPRESSION; NITRIC-OXIDE; BLOOD-FLOW; VASODILATOR PRODUCTION; SYSTEMIC ARTERIES; ARGININE SUPPLEMENTATION;
D O I
10.1387/ijdb.082799lr
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
The importance of the placenta and its vascular development to fetal growth and development has been appreciated since ancient times. Based on numerous studies in humans and animal model organisms in the last 2-3 decades, normal placental angiogenesis is critically important to ensure adequate blood flow to the placenta and therefore to provide the substrates that support normal fetal growth. Placental angiogenesis is abnormal at term in compromised pregnancies (those in which fetal growth is altered), including those resulting from maternal nutritional or environmental stress, maternal age, increased numbers of fetuses, maternal or fetal genotype, or the use of assisted reproductive technologies (e.g., cloning by somatic cell nuclear transfer). We and others have recently shown that these defects in placental vascular development occur quite early in pregnancy and may therefore presage compromised fetal growth and development. The challenges will be to find biomarkers of abnormal placental angiogenesis and to develop therapeutic strategies to "rescue" placental vascular development and thus fetal growth in compromised pregnancies. Animal models will be essential in meeting these challenges.
引用
收藏
页码:355 / 365
页数:11
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