Maternal characteristics predisposing to fetal growth restriction

Fetal growth restriction affects up to 10% of live-born infants representing a major cause of neonatal morbidity and mortality worldwide, being a significant risk factor for future adult health. A reduction of nutrient supply and oxygenation is the final common basis in fetal growth restriction. However, mechanisms involved can be various, and depending both by external (maternal diet and environment – such as pollution, living at high altitude, maternal smoke-) and internal (maternal/placental/fetal altered metabolism or molecular mechanisms) causes. Impaired placental function is mainly the final step leading to decreased nutrient and oxygen transfer to the fetus. Indeed, the placenta has an active role in fetal nutrition. Maternal metabolism and state of health can represent a risk factor affecting placental function. Impaired maternal nutrition and nutrient uptake can alter nutrient supply to the fetus across the placenta. At the same time, maternal characteristics such as body mass index and lifestyle, can influence both systemic and local oxidative stress and inflammation, potentially conditioning fetal growth. In fetal growth restriction, maternal diet and environmental factors are very important causes of epigenetic modifications such as altered DNA methylation and microRNAs expression, leading to impaired placental function, with sexual dimorphism in the placental response to maternal environment. On the other side, fetal uptake and metabolism can affect fetal growth and energy production. A cross-talk between mother-placenta-fetus compartments, further complicates the identification of the possible origin of fetal growth deficiency. Any insult deriving from the environment or from one of these three compartments, affects their cross-talk, possibly leading to fetal growth restriction. In this context, it is of utmost importance to produce guidelines for preconception as well as for pregnancy monitoring, in order to reduce the potential negative effects of exposures that have an impact on fetal growth and on future epigenetic marks.