Extracellular Vesicles in Pregnancy Complications

Extracellular vesicles (EVs) are membrane-bound particles released by placental and maternal cells that mediate intercellular communication throughout gestation. These vesicles encompass exosomes, microvesicles and apoptotic bodies and carry diverse molecular cargo—including proteins, lipids, nucleic acids and bioactive lipids—that reflect the physiological state of their cell of origin. In healthy pregnancy, EVs support placental angiogenesis, immunotolerance and vascular adaptation. However, in complications such as preeclampsia, intrauterine growth restriction and gestational diabetes, both the quantity and molecular composition of circulating EVs are altered. Dysregulated EV release may exacerbate endothelial dysfunction by delivering anti-angiogenic factors or inflammatory RNA species to maternal endothelium, while placenta-derived EVs loaded with specific microRNAs or tRNA fragments can impair trophoblast invasion, foetal organogenesis and immune balance. Conversely, EVs from normotensive pregnancies have demonstrated protective effects against long-term cardiovascular sequelae. The dual potential of EVs as drivers of pathology and as accessible biomarkers has fostered interest in their diagnostic and therapeutic applications. Emerging research aims to harness their molecular signatures for early detection of pregnancy disorders and to explore the use of engineered or purified vesicles to restore vascular homeostasis, offering promise for personalised obstetric care.

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Extracellular Vesicles in Pregnancy Complications publication trend

The graph below shows the total number of articles in extracellular vesicles in pregnancy complications across all publications each year (not limited to Nature Index journals).

Technical terms

Extracellular vesicles (EVs): Lipid-bilayer particles secreted by cells that transport molecular cargo between cells, influencing physiology and pathology.

Exosomes: A subtype of EVs (30–150 nm) formed within endosomal compartments and released upon fusion of multivesicular bodies with the plasma membrane.

Microvesicles: EVs (100–1,000 nm) generated by direct outward budding of the plasma membrane, carrying membrane-associated proteins and cytosolic content.

Syncytiotrophoblast: The multinucleated outer layer of the placental villi in direct contact with maternal blood, a major source of placental EVs.

5′-tRNA fragments (5′-tRFs): Small RNA fragments derived from the 5′ end of transfer RNAs, implicated in stress responses and immune modulation.

Long noncoding RNAs (lncRNAs): RNA molecules exceeding 200 nucleotides that do not code for protein but regulate gene expression at transcriptional and post-transcriptional levels.

References

1. Preeclampsia impedes foetal kidney development by delivering placenta-derived exosomes to glomerular endothelial cells. Cell Communication and Signaling (2023).
2. Platelet and mitochondrial RNA is decreased in plasma-derived extracellular vesicles in women with preeclampsia—an exploratory study. BMC Medicine (2023).
3. Differential 5′-tRNA Fragment Expression in Circulating Preeclampsia Syncytiotrophoblast Vesicles Drives Macrophage Inflammation. Hypertension (2024).
4. Normotensive placental extracellular vesicles provide long-term protection against hypertension and cardiovascular disease. American Journal of Obstetrics and Gynecology (2023).