Role of Autophagy in Preeclampsia

Abstract

Autophagy is essential in cell death decisions and can protect cells by preventing them from undergoing apoptosis. Autophagy contributes to a variety of physiological processes, including cell differentiation and various functions in embryogenesis. Some studies reported that the expressions of autophagy-related (Atg) proteins are found in placentas. This review article was focusing on the autophagy process and some Atg proteins which are involved in human placentation, especially in preeclampsia cases, since it has been well known that abnormal placentation and placenta dysfunction has crucial role in its development. Preeclampsia cannot be related to a single cause and the underlying mechanism of it is still not clearly understood. Recent hypothesis regarding the cause of preeclampsia is more focused on the inadequate trophoblast invasion and placentation. Scientists also suggested that other mechanism might be associated with this condition in preeclampsia, which is autophagy. Autophagy is a mechanism that essential for cellular remodeling which occurs during the development of multicellular organisms in the special process, by expressing an “eat-me” signal and cleared by neighboring cells. In preeclampsia patients, autophagy has an important role in trophoblast function under physiologically low oxygen conditions. The activation of autophagy in preeclampsia is shown by the different level of abundance of key protein of the Atg pathway. Some Atg proteins known to be related to preeclampsia are Beclin-1, LC3, and p62.