Fetal growth is dependent on nutrient and oxygen availability, which in turn is related to maternal endowment and substrate transfer by the placenta into the fetal circulation. Indeed, any given substrate must traverse the placental blood barrier. Transfer across this physiological barrier is governed by placental size, morphology (surface area for exchange and thinness of the diffusion barrier separating the maternal and fetal circulations), vascularity, blood supply and nutrient transporter properties. Nutrient transporter systems and placental vascularization are modulated by the environment and the abundance of growth regulatory factors. Fascinatingly data emerging largely from work on experimental models indicate that placental vascularization, morphological maturation and transport function can adaptively increase in response to both intrinsic (fetal-placental growth genes, developmental program) and extrinsic factors (maternal nutrition, stress, other environmental cues) to maintain and/or optimize fetal substrate supply and fetal growth in the prevailing suboptimal environments. The type and extent of the placental response depends on the type, gestational timing and duration of the suboptimal condition and therefore suggest that in pathological situations, adaptive responses by the placenta fail to occur or are inadequate. In particular, placental vascularization and nutrient transport are reported to be reduced in pathological intrauterine growth restriction or preeclampsia, but they are increased during gestational diabetes and obesity. Articles in this Research Topic will endeavour to identify the involvement and possible cross-talk of nutrient transport systems and angiogenic pathways in the placenta in meeting fetal requirements for oxygen and nutrients under suboptimal and pathological conditions.
Fetal growth is dependent on nutrient and oxygen availability, which in turn is related to maternal endowment and substrate transfer by the placenta into the fetal circulation. Indeed, any given substrate must traverse the placental blood barrier. Transfer across this physiological barrier is governed by placental size, morphology (surface area for exchange and thinness of the diffusion barrier separating the maternal and fetal circulations), vascularity, blood supply and nutrient transporter properties. Nutrient transporter systems and placental vascularization are modulated by the environment and the abundance of growth regulatory factors. Fascinatingly data emerging largely from work on experimental models indicate that placental vascularization, morphological maturation and transport function can adaptively increase in response to both intrinsic (fetal-placental growth genes, developmental program) and extrinsic factors (maternal nutrition, stress, other environmental cues) to maintain and/or optimize fetal substrate supply and fetal growth in the prevailing suboptimal environments. The type and extent of the placental response depends on the type, gestational timing and duration of the suboptimal condition and therefore suggest that in pathological situations, adaptive responses by the placenta fail to occur or are inadequate. In particular, placental vascularization and nutrient transport are reported to be reduced in pathological intrauterine growth restriction or preeclampsia, but they are increased during gestational diabetes and obesity. Articles in this Research Topic will endeavour to identify the involvement and possible cross-talk of nutrient transport systems and angiogenic pathways in the placenta in meeting fetal requirements for oxygen and nutrients under suboptimal and pathological conditions.