The role of the placenta in the formation of gestational complications in women with metabolic syndrome

Abstract

Over the past decade, the prevalence of metabolic syndrome has increased significantly worldwide, and in most countries around the world this non-communicable disease has become a major health threat. Today, the mechanisms of metabolic syndrome influence on the development of various pregnancy complications are actively discussed. Studies of the pathophysiological mechanisms of the relationship between metabolic disorders and placental-associated pregnancy complications deserve special attention. The placenta performs essential functions throughout pregnancy and serves as a site for nutrient exchange and gas exchange between the pregnant woman and the fetus. Metabolic changes in women are closely associated with a number of placentally mediated obstetric complications, including preeclampsia, placental insufficiency, macrosomia, fetal growth restriction and antenatal fetal death. It is believed that it is in the first trimester of pregnancy that trophoblast cells are most sensitive to metabolic changes in homeostasis, which leads to their ischemia, impaired proliferation, invasion and angiogenesis. In pregnancies complicated by metabolic syndrome, the placenta is exposed to inflammation, oxidative stress, dyslipidemia, hyperglycemia, and altered hormone levels. Such metabolic changes can affect the development and function of the placenta, leading to abnormal fetal growth, as well as metabolic and cardiovascular disorders in children in the long term. Despite the wide range of pregnancy complications with metabolic syndrome, the mechanisms of their development have not been sufficiently studied. The purpose of this review was to summarize current knowledge about the pathophysiological mechanisms of the influence of metabolic syndrome on the development and function of the placenta.