[1] Decidualization plays an important role in promoting placenta formation between a mother and her fetus by mediating the invasiveness of trophoblast cells.

It also triggers the production of cellular and molecular factors that result in structural changes, or remodeling, of maternal spiral arteries.

Decidualization is required in some mammalian species where embryo implantation and trophoblast cell invasion of the endometrium occurs, also known as hemochorial placentation.

In the event no embryo is implanted, the decidualized endometrial lining is shed or, as is the case with species that follow the estrous cycle, absorbed.

The changes in the ESCs result in the endometrium developing a secretory lining that produces a variety of proteins, cytokines, and growth factors.

These secreted factors will regulate the invasiveness of trophoblast cells that eventually form the placental connection if an embryo implants into the decidua.

The increased production of these ECM proteins turns the endometrium into the dense structure known as the decidua, which produces factors that promote trophoblast attachment and inhibit overly aggressive invasion.