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Fetal programming and early identification of newborns at high risk of free radical-mediated diseases
Serafina Perrone1, Antonino Santacroce1, Anna Picardi1
1Serafina Perrone, Antonino Santacroce, Anna Picardi, Giuseppe Buonocore, Department of Molecular and Developmental Medicine, University of Siena, 53100 Siena, Italy.
Insights
Fetal programming, influenced by placental function during pregnancy, can lead to adult metabolic syndrome. Early detection of oxidative stress in fetuses and newborns is key to preventing future health issues.
Area of Science:
- Developmental biology
- Metabolic disorders
- Perinatal medicine
Background:
- Metabolic syndrome is a growing health concern with developmental origins.
- Pediatricians play a crucial role in addressing this condition.
- Fetal programming, disruption of normal fetal development, links early life events to adult diseases.
Purpose of the Study:
- To explore the role of the placenta in fetal programming.
- To understand the mechanisms linking placental dysfunction to metabolic syndrome.
- To identify potential interventions for preventing adult morbidity.
Main Methods:
- Review of experimental studies on fetal-placental perturbations.
- Analysis of the role of placental adaptive changes in programming.
- Investigation of oxidative stress as a unifying mechanism.
Main Results:
- Pregnancy complications (diabetes, pre-eclampsia, hypoxia) are linked to placental dysfunction.
- Fetal-placental perturbations predispose to adult metabolic syndrome, obesity, and cardiovascular disease.
- Oxidative stress is implicated as a key mechanism in fetal programming.
Conclusions:
- Placental dysfunction during critical intrauterine periods can program fetuses for metabolic syndrome.
- Oxidative stress is a likely mediator connecting placental issues to adverse health outcomes.
- Early identification of oxidative damage risk in neonates is vital for reducing long-term morbidity.
Abstract:
Nowadays metabolic syndrome represents a real outbreak affecting society. Paradoxically, pediatricians must feel involved in fighting this condition because of the latest evidences of developmental origins of adult diseases. Fetal programming occurs when the normal fetal development is disrupted by an abnormal insult applied to a critical point in intrauterine life. Placenta assumes a pivotal role in programming the fetal experience in utero due to the adaptive changes in structure and function. Pregnancy complications such as diabetes, intrauterine growth restriction, pre-eclampsia, and hypoxia are associated with placental dysfunction and programming. Many experimental studies have been conducted to explain the phenotypic consequences of fetal-placental perturbations that predispose to the genesis of metabolic syndrome, obesity, diabetes, hyperinsulinemia, hypertension, and cardiovascular disease in adulthood. In recent years, elucidating the mechanisms involved in such kind of process has become the challenge of scientific research. Oxidative stress may be the general underlying mechanism that links altered placental function to fetal programming. Maternal diabetes, prenatal hypoxic/ischaemic events, inflammatory/infective insults are specific triggers for an acute increase in free radicals generation. Early identification of fetuses and newborns at high risk of oxidative damage may be crucial to decrease infant and adult morbidity.
