Extracellular vesicles in preeclampsia: drivers of vascular dysfunction and inflammation

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Vascular inflammation, augmented vasoconstriction, reduced vasodilatory capacity, and endothelial dysfunction are cardinal features of the maternal vascular dysfunction phenotype in preeclampsia. Extracellular vesicles (EVs), bioactive molecules loaded with proteins, glycans, lipids, and nucleic acids facilitate intracellular signaling and cell-to-cell cross talk. Circulating EV concentrations rise throughout normal pregnancy; however, preeclampsia is characterized by a further increase in multiple types of EVs and a shift toward a proinflammatory, vasoactive cargo. Emerging evidence suggests that in preeclampsia, circulating EVs activate maternal endothelial cells, propagate vascular inflammation, and impair vascular tone and endothelial integrity, contributing to the development of hypertension and excess vasoconstriction. This review briefly introduces fundamental knowledge about EV biogenesis, morphology, and cargo selection, then focuses on current evidence on EV-induced endothelial inflammation and vascular dysfunction in pregnancies with preeclampsia versus uncomplicated pregnancies. Finally, we discuss the therapeutic potential of engineered or stem cell-derived EVs to restore maternal vascular health in preeclampsia.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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