The article reviews the impact of maternal obesity on placental inflammation and oxidative stress, and their consequences for fetal development and health. Maternal obesity is a significant risk factor for adverse pregnancy outcomes, including spontaneous abortion, stillbirth, gestational hypertension, abnormal birthweight, and gestational diabetes. Inflammation and oxidative stress are key mediators of these effects, with obesity-induced chronic low-grade inflammation and increased reactive oxygen species (ROS) production contributing to placental dysfunction. The placenta, which plays a crucial role in modulating the intrauterine environment and fetal development, is particularly affected by these mechanisms. Human and animal studies have shown that maternal obesity is associated with increased placental inflammation, oxidative stress, and altered lipid handling, which can lead to adverse fetal outcomes such as fetal growth restriction (FGR), preterm birth, and increased risk of metabolic diseases in offspring. The review highlights the need for further research to understand the mechanisms underlying these effects and to develop interventions that can mitigate their adverse impacts. Potential strategies include maternal exercise, dietary modifications, and the use of natural products with antioxidant and anti-inflammatory properties. The article also discusses the epigenetic mechanisms that may contribute to the long-term health effects of maternal obesity on offspring, emphasizing the importance of sex-specific responses and the role of parental factors.The article reviews the impact of maternal obesity on placental inflammation and oxidative stress, and their consequences for fetal development and health. Maternal obesity is a significant risk factor for adverse pregnancy outcomes, including spontaneous abortion, stillbirth, gestational hypertension, abnormal birthweight, and gestational diabetes. Inflammation and oxidative stress are key mediators of these effects, with obesity-induced chronic low-grade inflammation and increased reactive oxygen species (ROS) production contributing to placental dysfunction. The placenta, which plays a crucial role in modulating the intrauterine environment and fetal development, is particularly affected by these mechanisms. Human and animal studies have shown that maternal obesity is associated with increased placental inflammation, oxidative stress, and altered lipid handling, which can lead to adverse fetal outcomes such as fetal growth restriction (FGR), preterm birth, and increased risk of metabolic diseases in offspring. The review highlights the need for further research to understand the mechanisms underlying these effects and to develop interventions that can mitigate their adverse impacts. Potential strategies include maternal exercise, dietary modifications, and the use of natural products with antioxidant and anti-inflammatory properties. The article also discusses the epigenetic mechanisms that may contribute to the long-term health effects of maternal obesity on offspring, emphasizing the importance of sex-specific responses and the role of parental factors.