Placental inflammation, oxidative stress, and fetal outcomes in maternal obesity

Placental inflammation, oxidative stress, and fetal outcomes in maternal obesity

July 2024 | Cindy X.W. Zhang, Alejandro A. Candia, and Amanda N. Sferruzzi-Perri
Maternal obesity during pregnancy is associated with increased placental inflammation, oxidative stress, and altered placental function, which can negatively impact fetal outcomes. This review summarizes recent research on the mechanisms linking maternal obesity to placental and fetal health. Maternal obesity is linked to chronic low-grade inflammation and increased reactive oxygen species (ROS), which can disrupt placental function and fetal development. The placenta, a critical organ for fetal growth and nutrient transfer, is affected by these changes, leading to increased risk of preterm birth, fetal growth restriction, and long-term metabolic disorders in offspring. Inflammation and oxidative stress are central to the adverse effects of maternal obesity. Inflammatory cytokines such as TNFα and IL-6, along with increased ROS, contribute to placental dysfunction and fetal complications. Human and animal studies show that maternal obesity is associated with placental inflammation, altered immune responses, and increased oxidative stress. These changes can lead to programmed metabolic and immune alterations in offspring, with sex-specific effects observed. Maternal obesity also affects fetal growth and development, with both macrosomia and fetal growth restriction reported. Offspring of obese mothers show increased adiposity, metabolic syndrome, and altered immune responses. Lifestyle interventions such as increased physical activity and serine supplementation have shown promise in mitigating oxidative stress and inflammation in the placenta and offspring. Epigenetic mechanisms, including DNA methylation and miRNA expression, may play a role in the long-term effects of maternal obesity on offspring. Future research should focus on understanding the interplay between maternal obesity, placental function, and fetal outcomes, as well as the potential for therapeutic interventions to improve placental health and reduce adverse fetal outcomes. The review highlights the need for further studies to explore the impact of maternal obesity on immune and oxidative stress pathways in the placenta and offspring, and to develop effective strategies for prevention and intervention.Maternal obesity during pregnancy is associated with increased placental inflammation, oxidative stress, and altered placental function, which can negatively impact fetal outcomes. This review summarizes recent research on the mechanisms linking maternal obesity to placental and fetal health. Maternal obesity is linked to chronic low-grade inflammation and increased reactive oxygen species (ROS), which can disrupt placental function and fetal development. The placenta, a critical organ for fetal growth and nutrient transfer, is affected by these changes, leading to increased risk of preterm birth, fetal growth restriction, and long-term metabolic disorders in offspring. Inflammation and oxidative stress are central to the adverse effects of maternal obesity. Inflammatory cytokines such as TNFα and IL-6, along with increased ROS, contribute to placental dysfunction and fetal complications. Human and animal studies show that maternal obesity is associated with placental inflammation, altered immune responses, and increased oxidative stress. These changes can lead to programmed metabolic and immune alterations in offspring, with sex-specific effects observed. Maternal obesity also affects fetal growth and development, with both macrosomia and fetal growth restriction reported. Offspring of obese mothers show increased adiposity, metabolic syndrome, and altered immune responses. Lifestyle interventions such as increased physical activity and serine supplementation have shown promise in mitigating oxidative stress and inflammation in the placenta and offspring. Epigenetic mechanisms, including DNA methylation and miRNA expression, may play a role in the long-term effects of maternal obesity on offspring. Future research should focus on understanding the interplay between maternal obesity, placental function, and fetal outcomes, as well as the potential for therapeutic interventions to improve placental health and reduce adverse fetal outcomes. The review highlights the need for further studies to explore the impact of maternal obesity on immune and oxidative stress pathways in the placenta and offspring, and to develop effective strategies for prevention and intervention.
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