Autophagy is an evolutionarily conserved process in eukaryotes by which cytoplasmic cargo sequestered inside double-membrane vesicles is delivered to the lysosome for degradation. In early pregnancy, trophoblasts and the fetus experience hypoxic and low-nutrient conditions; nevertheless, extravillous trophoblasts (EVTs) invade the uterine myometrium up to one-third of its depth and migrate along the lumina of spiral arterioles, replacing the maternal endothelial lining. An enhancement of autophagy induced by physiological hypoxia takes part in the invasion and vascular remodeling in EVTs. On the other hand, soluble endoglin, which increased in sera in preeclamptic cases, suppresses EVT-invasion or -vascular remodeling by inhibiting autophagy In vitro. In addition, a substance selectively degraded by autophagy, p62/SQSTM1, accumulates in EVT cells in preeclamptic placental biopsy samples showing impaired autophagy in vivo. Thus, alternation of autophagy could affect fates of mothers and babies. Recently increasing evidence of modulating autophagy has accumulated during pregnancy. In this chapter, we introduce the role of autophagy in embryogenesis, implantation, and maintaining pregnancy.
Part of the book: Autophagy in Current Trends in Cellular Physiology and Pathology