Figure 8

Proposed model for the potential implication of NKX3.1 in the pathogenesis of fetal growth restriction (FGR) by the end of the first trimester. Lack of maintenance of EG-VEGF has been associated with FGR (16–19). An EG-VEGF increase could lead to abnormal downregulation of NKX3.1 expression leading to an increase in trophoblast differentiation, apoptosis and shedding as well as sustained inhibition of extravillous trophoblast (EVCT) invasion. The failure in spiral arteriole remodeling, known to be associated with FGR, would therefore contribute to abnormal persistence of placental hypoxia in the intervillous space, and could then act as a positive feedback loop to exacerbate EG- VEGF production.