AIM: Preeclampsia (PE) is a severe pregnancy-related disorder characterized by hypertension and multi-organ failure, primarily affecting the maternal vasculature and placenta. The aim of this review is to explain the molecular mechanisms behind PE by investigating the relationship between exosome release and complement activation, which could provide insight into potential therapeutic targets. METHODS: This review analyzes existing literature on the role of the complement system and exosomes in the pathophysiology of PE. The focus is on how abnormal complement activation contributes to inflammation and vascular dysfunction, particularly in the placenta, and the role of trophoblast-derived exosomes carrying pathogenic molecules such as soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng). RESULTS: Findings from recent studies indicate that during PE, abnormal complement activation leads to severe inflammation and vascular dysfunction in the placenta. Additionally, exosomes, particularly those derived from trophoblasts, are present in higher concentrations in maternal circulation during PE and carry molecules that disrupt endothelial function. These factors contribute to the development of hypertension and other maternal complications. CONCLUSIONS: Understanding the interaction between complement activation and exosome release in PE may open avenues for novel therapeutic approaches. Targeting complement regulation and exosome-mediated signaling could potentially improve maternal and fetal outcomes, offering new strategies for managing this complex condition.