Exploring the impact of Apelin and Reactive Oxygen Species on autophagy and cell senescence in pre-eclampsia.

This research investigates the interplay between Reactive Oxygen Species (ROS) and Apelin (APLN) in regulating autophagy, with implications for placental cell senescence and apoptosis in pre-eclampsia (PE). We manipulated APLN expression using sgRNA to study its effects on ROS levels and subsequent cellular responses. Our findings reveal that APLN overexpression elevates ROS production, accelerating cellular senescence and apoptosis. In contrast, silencing APLN enhances autophagy, thereby diminishing cellular aging and apoptosis. These outcomes were confirmed in vitro and in vivo experiments, establishing a causative relationship between ROS-mediated APLN modulation and altered placental cell dynamics in PE. The results suggest potential therapeutic targets within the ROS and APLN pathways to alleviate detrimental changes in the placenta, offering new strategies for the clinical management of PE. This study emphasizes the crucial role of autophagy in placental health and sets the stage for future investigations into therapeutic interventions for pregnancy-related complications.