Genomic Insights at the Maternal-Fetal Interface: Preeclampsia Subtypes and Clinical Implications

Recent advances in single-cell transcriptomics have provided significant insights into the pathophysiology of preeclampsia, uncovering cell-type-specific gene expression changes at the maternal-fetal interface. Key discoveries include dysregulated angiogenic factors, such as elevated sFlt-1 (soluble fms-like tyrosine kinase-1) and reduced PlGF (placental growth factor), predominantly in syncytiotrophoblasts, alongside inflammatory and stress-related signatures in stromal and immune cells. These findings reinforce the clinically observed concept of 2 distinct preeclampsia subtypes: a placenta-dominant form and a maternal cardiovascular-dominant form, each characterized by unique etiologies, clinical presentations, and therapeutic implications. Ongoing genomic research has the potential to identify novel biomarkers and therapeutic targets, paving the way for improved screening and management strategies for this multifaceted condition.