期刊
INTERNATIONAL JOURNAL OF DEVELOPMENTAL BIOLOGY
卷 58, 期 2-4, 页码 247-259出版社
UNIV BASQUE COUNTRY UPV-EHU PRESS
DOI: 10.1387/ijdb.140083ms
关键词
hemochorial placentation; natural killer cell; trophoblast; PI3K/AKT; FOSL1; hypoxia; NOTCH; STOX1
资金
- National Institutes of Health [HD020676, HD072100]
- American Heart Association
- Japan Society for the Promotion of Science
- Canadian Institutes of Health Research
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [R01HD020676, P30HD002528, R03HD072100, P01HD079363] Funding Source: NIH RePORTER
Implantation of the embryo into the uterus triggers the initiation of hemochorial placentation. The hemochorial placenta facilitates the acquisition of maternal resources required for embryo/fetal growth. Uterine spiral arteries form the nutrient supply line for the placenta and fetus. This vascular conduit undergoes gestation stage-specific remodeling directed by maternal natural killer cells and embryo-derived invasive trophoblast lineages. The placentation site, including remodeling of the uterine spiral arteries, is shaped by environmental challenges. In this review, we discuss the cellular participants controlling pregnancy-dependent uterine spiral artery remodeling and mechanisms responsible for their development and function.
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