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The study aimed to investigate the changes in small extracellular vesicles (sEVs) in venous malformations (VMs) and understand their role in intercellular communication. Fifteen VM patients and twelve healthy donors were included in the study. The researchers isolated sEVs from VM lesion tissues and cell supernatants and analyzed them using various techniques. They found that the size of sEVs from VM tissues and cell models was significantly increased. They identified VPS4B, a regulator of sEV size, which was downregulated in VM endothelial cells. Abnormal activation of the AKT signaling pathway was responsible for the downregulation of VPS4B and the increased size of sEVs. Restoring normal AKT activation levels corrected the size change of sEVs by increasing VPS4B expression. These findings suggest that dysregulated sEVs may play a role in the development of VMs.
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