Malaria in pregnancy is a major public health problem in countries where the disease is endemic, causing maternal and infant morbidity and mortality. It remains unclear why pregnant women are more susceptible to malaria. However, it is known that the placenta provides a favorable environment to the development of certain parasite subpopulations, triggering an intense inflammatory infiltrate which is associated with abortions, intrauterine growth retardation, premature births and low birth weight. Autophagy is an essential process for cell survival during stress, such as infections or cell exposure to microbial products. It also plays a role in the trophoblast response to stress agents in normal pregnancy, allowing these cells to adapt to a variety of insults usually found in pregnant women. Certain signaling molecules related to the immune system can regulate autophagy. Although in recent years many studies have defined the clinical manifestations of malaria during pregnancy, the cellular and molecular mechanisms associated with the inflammatory process are not yet fully understood. In this project we intend to evaluate the role of autophagy in the pathogenesis of placental malaria. This study will not only make an important contribution to a better understanding of placental malaria, but could also enable new studies directed to the development of new diagnostic methods and gestational malaria treatment.
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