Thyroid hormones (THs) regulate a number of metabolic processes during pregnancy. After implantation, the placenta forms and enhances embryonic growth and development. Dysregulated maternal THs signaling has been observed in malplacentation-mediated pregnancy complications such as preeclampsia, miscarriage, and intrauterine growth restriction (IUGR), but the molecular mechanisms involved in this association have not been fully characterized. In this review, we have discussed THs signaling and its roles in trophoblast proliferation, trophoblast differentiation, trophoblast invasion of the decidua, and decidual angiogenesis. We have also explored the relationship between specific pregnancy complications and placental THs transporters, deiodinases, and THs receptors. In addition, we have examined the effects of specific endocrine disruptors on placental THs signaling. The available evidence indicates that THs signaling is involved in the formation and functioning of the placenta and serves as the basis for understanding the pathogenesis and pathophysiology of dysthyroidism-associated pregnancy complications such as preeclampsia, miscarriage, and IUGR.

Summary sentence

Normal THs signaling promotes placentation; while abnormal THs signaling leads to malplacentation and its associated pregnancy complications, such as preeclampsia, miscarriage and IUGR.