Affiliations: Department of Pediatrics, Dr. Peset University
Hospital, Valencia, Spain | Department of Pediatrics, Obstetrics and Gynecology,
University of Valencia, Valencia, Spain
Note: [] Corresponding author: Pilar Codoñer-Franch, Department of
Pediatrics, Dr. Peset University Hospital, Avenida Gaspar Aguilar 90, 46017
Valencia, Spain. Tel.: +34 96 1622389; Fax: +34 96 3864815; E-mail: [email protected]
Abstract: Intrauterine growth retardation (IUGR) is the failure of the fetus
to achieve his/her intrinsic growth potential, due to anatomical and/or
functional disorders and diseases in the feto-placental-maternal unit. Fetal
growth within the uterus is a complex biological event influenced by genetic,
epigenetic, and environmental factors, as well as maternal nutrition. These
factors impact on the size and functional capacity of the placenta,
uteroplacental blood flows and transfer of nutrients and oxygen from mother to
fetus. Oxidative stress can influence metabolic pathways that alter the
epigenetic state (stable alterations of gene expression through DNA methylation
and histone modifications) of the fetal genome. This may provide a molecular
mechanism for the role of oxidative stress on fetal programming. IUGR results
in significant perinatal and long-term complications, including the development
of insulin resistance/metabolic syndrome in adulthood. By linking oxidative
stress with dysregulation of specific target genes, we may be able to develop
therapeutic strategies that protect against organ dysfunction in the programmed
offspring.