Fetal Pediatr Pathol. 2025 Sep 19:1-10. doi: 10.1080/15513815.2025.2558605. Online ahead of print.
ABSTRACT
Preeclampsia (PE) remains a leading cause of maternal and neonatal morbidity and mortality globally. Among several experimental models developed to interrogate the pathogenesis of PE, the mouse model employing systemic infusion or transgenic overexpression of soluble fms-like tyrosine kinase-1 (sFlt1) has gained widespread use due to its capacity to induce cardinal features of the human disease. These include maternal hypertension, renal injury, endothelial dysfunction, placental abnormalities, fetal growth restriction, and adverse long-term outcomes. This review critically evaluates the sFlt1-based mouse model of PE, highlighting its utility for understanding the pathogenesis of angiogenic imbalance and its sequelae. We contrast findings from this model with clinical observations in human PE and discuss applications for studying early-onset versus late-onset forms. Finally, we address limitations and propose strategies to enhance its translational relevance. Placing the model in the context of human disease helps guide its use in future preclinical and translational research.
PMID:40970739 | DOI:10.1080/15513815.2025.2558605
