Placental Development and Pregnancy-Associated Diseases

Abstract

Serving as the interface between the fetal and maternal environments during gestation, the placenta plays critical roles in the protection of the developing fetus and the maintenance of maternal health. The placenta is primarily derived from the embryonic trophectoderm which differentiates into various subtypes of trophoblast cells through villous and extravillous pathways. The interactions among trophoblasts and multiple decidual cells and immune cells at the maternal-fetal interface fundamentally form the functional units of the placenta, which are responsible for blood perfusion and maternal-fetal material exchange, immune tolerance, and the regulation of pregnancy adaptation. Defects in placental development and functional maintenance are in tight association with adverse pregnancy outcomes such as preeclampsia. In this article, we review recent advances on human trophoblast cell differentiation and the construction of placental functional units and discuss the placental and maternal factors that may contribute to the occurrence of preeclampsia.

Endocytosis at the maternal-fetal interface: balancing nutrient transport and pathogen defense

“…The well-organized differentiation of trophoblasts and the complex interactions among trophoblasts and a multitude of maternal cells at the maternal-fetal interface results in the formation of several functional units. The first unit involves the uterine decidua, where the interactions among decidual stromal cells, maternal immune cells, and trophoblast cells of fetal origin ensure immune tolerance to the semi-allogenic fetus, while protect against placental/fetal infections ( 2 , 3 , 5 ). The second functional unit is the placental villi, which are fundamental for maternal-fetal material exchange.…”

“…A successful pregnancy necessitates a continuous dialogue between the mother and developing conceptus. This communication is facilitated by intricate interactions between maternal and fetal cells at specific sites in the uterus, collectively referred to as the “maternal-fetal interface.” The placenta plays an instrumental role in fetal growth and health by enabling nutrient uptake from the mother’s blood, facilitating waste removal from the fetus’s blood, ensuring immunological tolerance for the semi-allogenic fetus, and acting as a protective barrier against toxins and pathogens ( 1 – 3 ). The distribution of nutrients between the mother and fetus during pregnancy is predominantly influenced by these maternal-fetal interactions, which are largely regulated by the placenta.…”

Placental galectins: a subfamily of galectins lose the ability to bind β-galactosides with new structural features

“…Taken together, placental galectins act to modulate trophoblast cell functions and immune tolerance at the maternal-fetal interface. Dysfunctions of trophoblastic cells and imbalanced immunity at the maternal-fetal interface are the causes of many pregnancy diseases such as gestational diabetes mellitus (GDM), pre-eclampsia (PE), intrauterine growth restriction (IUGR), and HELLP syndrome [87, 90]. Therefore, placental galectins are speculated to be important pathogenic factors and therapeutic targets in these diseases.…”

The Mother–Child Dyad Adipokine Pattern: A Review of Current Knowledge

“…During pregnancy, maternal insulin resistance increases and might translate to the increased transport of glucose and amino acids and fatty acids across the placenta [ 27 ]. The development and maturation of the placenta is disturbed as a result of maternal-impaired glucose metabolism, and it leads to vascular dysfunction, including increased angiogenesis, villous fibrinoid necrosis [ 31 , 32 , 33 , 34 ], and changes associated with inflammation and oxidative stress that can lead to chronic fetal hypoxia [ 35 ]. Finally, maternal hyperglycemia might induce an increase in fetal insulin resistance and translate into its disturbed growth [ 28 , 36 , 37 , 38 ] as well as a long-term health risk for infants [ 27 ].…”