We are dedicated to the study of transport mechanisms in the human placenta and their alterations in pathological conditions.
The placenta is an organ that mediates between the mother and the fetus, allowing the exchange of gases and nutrients to ensure the baby's growth, protect it from infections and potentially harmful substances, provide support and mechanical protection, and offer the appropriate microenvironment for the normal development and growth within the mother. However, under certain circumstances, it can be the origin of serious pathological alterations in the mother and/or the fetus. One of these pathologies is Preeclampsia.
Preeclampsia is an exclusive disorder of human gestation, with an incidence causing significant maternal and fetal morbidity and mortality. It occurs in all populations with a general incidence varying between 5 and 7%. According to estimates from the WHO, preeclampsia is responsible for more than 200,000 maternal deaths per year worldwide and is associated with a 20-fold increase in perinatal mortality. In Argentina, preeclampsia accounts for 13.2% of all pathological pregnancies. According to data published by the Ministry of Health in 2010, hypertensive disorders, along with hemorrhages and infections, are the main causes of maternal morbidity and mortality.
Despite its importance in terms of public health and decades of research, the pathogenic mechanisms involving its development and progression are not fully determined. It is currently defined solely by the presence of clinical symptoms, making its diagnosis relatively weak, and prediction is not possible yet.
Many studies point to the placenta as a necessary participant in the pathogenesis of preeclampsia, as the disease generally resolves within 24-48 hours after its expulsion. Although the exact role of the placenta in the development of this gestational disorder is not yet fully understood, it is known that defective placentation is one of its main characteristics. Our main interest is focused on regulating the expression and functionality of placental transporters to establish new hypotheses that allow us to understand the mechanisms involved in the establishment of this gestational disorder.