he placenta – a pinnacle of morphological and functional perfection – coordinates complex biological demands necessary for a healthy pregnancy. Despite research, many pregnancy disorders still have an unclear etiology. Impaired transfer of nutrients and oxygen across the placenta highlights the crucial role of mitochondrial function in trophoblasts, the metabolic core of the placenta, suggesting mitochondrial function in trophoblasts may be key to understand these issues.Current theories on the pathophysiological mechanisms of placental insufficiencies focus on impaired oxidative phosphorylation and consequent mitochondrial damage, emphasizing the importance of mitochondrial quality control in placental homeostasis. However, mitochondrial characteristics in preeclamptic placentas, the most common insufficiency, point to the existence of an alternative mitochondrial mechanism that regulates trophoblast differentiation, a key process in placental development.This project focuses on investigating selective mitochondrial autophagy – mitophagy – as a novel mechanism of mitochondrial quality control in trophoblast differentiation. Using robust methodologies for transcriptomic and proteomic profiling of placental cells, the goal is to provide insights into the mechanisms of mitophagy during placentogenesis in both healthy and preeclamptic placentas. This integrated approach, combining human sample, mouse models, and trophoblast cell lines, will enhance our understanding of the role of mitophagy in placentogenesis and the pathophysiology of placental insufficiencies.Autophagy has become the subject of intensive research due to its role in the pathogenesis of numerous diseases. In this context, there is also the potential to modify autophagy as a therapeutic strategy. Therefore, investigating the molecular mechanisms of mitophagy may pave the way for new therapeutic approaches for treating placental insufficiencies, for which there is currently no effective therapy.