Am J Reprod Immunol. 2026 Aug;96(2):e70299. doi: 10.1111/aji.70299.
ABSTRACT
Preeclampsia (PE), a hypertensive disorder of pregnancy, is one of the leading causes of maternal and fetal mortality worldwide. Beyond the immediate pregnancy impact, it is also associated with increased long-term risks in both the mother and the offspring. Currently, no causal therapy exists. Consequently, the complex and heterogeneous nature of PE necessitates the exploration of novel therapeutic targets to improve maternal and fetal outcomes. This review summarizes models of pathogenesis in PE, particularly the two-stage model of the development of PE, where the placenta is suggested to be the main source of the disease, and the postulation that PE is a result of dysfunction of the maternal cardiovascular system. We explore novel therapeutic approaches, considering the underlying mechanisms such as galectin-13, placental growth factor, therapeutic plasma exchange (TPE), trophoblast-targeted nanomedicine, gene therapy, nitric oxide donors, endothelin receptor antagonists, and mesenchymal stem cells. Challenges in translating preclinical findings to clinical practice, including animal model limitations and ethical considerations, are discussed. Finally, this review integrates current treatment options, discusses their limitations, highlights ethical considerations, and outlines future directions for PE therapeutics, emphasizing the need for personalized therapeutic strategies.
PMID:42638178 | DOI:10.1111/aji.70299