The human placenta plays a central role in the development and growth of the fetus, as well as in the origin of multiple adult diseases.
The notion of the fetal origins of adult disease was first put forth by the British epidemiologist David Barker in 1986. Barker's theory ensures that both, high and low birth weights are indicators that show the connection between an adverse intrauterine environment and the likelihood that these fetuses would develop cardiovascular disease, obesity, and metabolic syndrome in adult life.
In this way, Diabetes mellitus, obesity, and cardiovascular diseases, among others, have their origin in the uterus where the placenta plays a fundamental role. There is general agreement that maternal stress during pregnancy is linked to poor outcomes for the fetus. Thus, an adverse fetal environment as a consequence of variations in the placental microbiome, exposure to toxic substances, maternal metabolic disorders, and placental alterations induce epigenetic changes that will influence the rest of life.
To date, numerous studies have connected maternal stress to the onset of cardiometabolic diseases in the offspring later in life.
Furthermore, programming effects may not be limited to the first generation directly exposed but may be transmitted to subsequent generations. Fetal programming is thought to act as an adaptive mechanism of the fetus to the intrauterine microenvironment. Although today it is also known that there are strategies to be able to reverse the programming processes.
Fetal programming is an adaptation process that modifies developmental pathways during the prenatal growth phase because of diet and other environmental influences. This results in altered metabolism and increased vulnerability to chronic disease in adults. In the last 50 years, a concept known as "developmental origins of health and disease" (DOHaD) has arisen, which connects early environmental factors to health status and illness risk in later childhood and adulthood. Originating from epidemiological findings, the idea has spawned a field that combines clinical research in a range of specialties, public and global health, experimental physiology, molecular biology (especially epigenetics), developmental biology, anthropology, social sciences, and evolutionary biology.
This Research Topic aims to analyze, discuss, and understand the role of the placenta as a determinant of the future health of the offspring. We welcome articles focusing on, but not limited to:
- Epigenetics and Fetal Programming.
- Maternal Nutrition and Epigenetics.
- Transcriptome and epigenome of trophoblast.
- Environment-epigenome interactions and role of placental genetic imprinting.
- Role of the placenta in fetal programming of adult chronic diseases.
- Developmental Origins of Health and Disease (DOHaD): Metabolic and Placental Syndromes - short-term and long-term effects on mother and offspring.
- Alterations in the placental microbiome.
- The placenta and fetal drug exposure.
- Animal and cell models for the study of pregnancy pathologies.
The human placenta plays a central role in the development and growth of the fetus, as well as in the origin of multiple adult diseases.
The notion of the fetal origins of adult disease was first put forth by the British epidemiologist David Barker in 1986. Barker's theory ensures that both, high and low birth weights are indicators that show the connection between an adverse intrauterine environment and the likelihood that these fetuses would develop cardiovascular disease, obesity, and metabolic syndrome in adult life.
In this way, Diabetes mellitus, obesity, and cardiovascular diseases, among others, have their origin in the uterus where the placenta plays a fundamental role. There is general agreement that maternal stress during pregnancy is linked to poor outcomes for the fetus. Thus, an adverse fetal environment as a consequence of variations in the placental microbiome, exposure to toxic substances, maternal metabolic disorders, and placental alterations induce epigenetic changes that will influence the rest of life.
To date, numerous studies have connected maternal stress to the onset of cardiometabolic diseases in the offspring later in life.
Furthermore, programming effects may not be limited to the first generation directly exposed but may be transmitted to subsequent generations. Fetal programming is thought to act as an adaptive mechanism of the fetus to the intrauterine microenvironment. Although today it is also known that there are strategies to be able to reverse the programming processes.
Fetal programming is an adaptation process that modifies developmental pathways during the prenatal growth phase because of diet and other environmental influences. This results in altered metabolism and increased vulnerability to chronic disease in adults. In the last 50 years, a concept known as "developmental origins of health and disease" (DOHaD) has arisen, which connects early environmental factors to health status and illness risk in later childhood and adulthood. Originating from epidemiological findings, the idea has spawned a field that combines clinical research in a range of specialties, public and global health, experimental physiology, molecular biology (especially epigenetics), developmental biology, anthropology, social sciences, and evolutionary biology.
This Research Topic aims to analyze, discuss, and understand the role of the placenta as a determinant of the future health of the offspring. We welcome articles focusing on, but not limited to:
- Epigenetics and Fetal Programming.
- Maternal Nutrition and Epigenetics.
- Transcriptome and epigenome of trophoblast.
- Environment-epigenome interactions and role of placental genetic imprinting.
- Role of the placenta in fetal programming of adult chronic diseases.
- Developmental Origins of Health and Disease (DOHaD): Metabolic and Placental Syndromes - short-term and long-term effects on mother and offspring.
- Alterations in the placental microbiome.
- The placenta and fetal drug exposure.
- Animal and cell models for the study of pregnancy pathologies.