ABSTRACT
The success of normal pregnancy depends on the protection, controlled invasion, and growth of the semiallogenic placenta within the maternal uterine environment. In the endometrium, the maternal response to pregnancy is characterized by influx of specialized uterine natural killer (uNK) cells, remodeling of the spiral arteries, and differentiation of the endometrial stromal cells (ESCs) into decidual cells. In most species, this maternal uterine response, termed decidualization, is
triggered by signals derived from the implanting blastocyst. In humans, however, the decidual process occurs independently of pregnancy during the midsecretory phase of each cycle. This apparent switch from embryonic to maternal control of the decidual process has profound consequences for human reproduction. For instance, ‘spontaneous’ or conceptus-independent decidualization of the endometrium also occurs in the few other species that menstruate, such as Old World monkeys, the elephant shrew (Elephantus myuras jamesoni), and certain bats, suggesting that these processes are
causally linked.1 Cyclic decidualization and menstrual shedding occur on average 400 times during the reproductive years of women in developed countries. Consequently, abnormal uterine bleeding is one of the most common disorders in women and a major indication for surgical intervention. Furthermore, emerging evidence suggests that reproductive disorders that affect the preconceptual endometrial milieu predispose to a spectrum of pregnancy complications associated with impaired trophoblast invasion, including miscarriage, preeclampsia, fetal growth restriction, and preterm labor.2
