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Role of the placenta in fetal programming: underlying mechanisms and potential interventional approaches
Thomas Jansson1, Theresa L Powell
1Department of Obstetrics and Gynecology, College of Medicine, University of Cincinnati, Cincinnati, OH 45267, USA. thomas.jansson@uc.edu
Clinical Science (London, England : 1979)
|June 1, 2007
Summary
Maternal factors during pregnancy can program fetal development, increasing risks for adult cardiovascular disease and diabetes. The placenta plays a key role in mediating these effects through nutrient sensing and hormonal regulation.
Area of Science:
- Developmental biology
- Reproductive medicine
- Endocrinology
Background:
- Adverse maternal conditions during fetal development can lead to long-term health risks, including cardiovascular disease and diabetes.
- The placenta is a crucial interface mediating maternal-fetal communication and environmental influences.
Purpose of the Study:
- To review how the placenta responds to maternal environmental changes and mediates fetal programming.
- To discuss mechanisms by which placental function influences offspring's long-term health.
Main Methods:
- Review of recent scientific literature on placental function and fetal programming.
- Analysis of mechanisms linking placental alterations to offspring disease risk.
Main Results:
- Placental vascular resistance in intrauterine growth restriction (IUGR) increases fetal cardiac workload, linking placental structure to cardiovascular programming.
- Reduced placental 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD-2) activity increases fetal cortisol exposure, programming hypertension and metabolic disease.
- The placenta acts as a nutrient sensor, regulating transport and influencing fetal growth and programming.
Conclusions:
- The placenta is central to fetal programming, directly regulating nutrient supply and fetal growth.
- Maternal perturbations can alter placental gene methylation and increase oxidative stress, impacting placental function.
- Interventions targeting placental growth, nutrient transport, or maternal factors like IGFs and methyl donors may prevent adverse fetal programming.
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