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Extracellular vesicle (EV) uptake is a complex biological process by which cells internalize membrane-bound vesicles, such as exosomes and microvesicles, released by other cells (Mulcahy et al., 2014). This process facilitates the horizontal transfer of bioactive molecules, including proteins, lipids, and various RNA species, thereby modulating the phenotype and function of recipient cells (van Niel et al., 2018). While EV uptake is critical for normal physiological communication and tissue homeostasis, it is also heavily implicated in the progression of various diseases, including cancer metastasis and the spread of neurodegenerative proteins (Kalluri & LeBleu, 2020). The term "Multiple cellular and molecular pathways via extracellular vesicle uptake" refers to the diverse array of endocytic mechanisms—such as macropinocytosis, clathrin-mediated endocytosis, and phagocytosis—and specific receptor-ligand interactions that mediate this internalization (Costa Verdera et al., 2017). Because this describes a broad biological phenomenon involving numerous distinct molecular players rather than a single protein or receptor, it is not considered a discrete therapeutic target in the traditional sense. However, specific components of these pathways, such as heparan sulfate proteoglycans or integrins, are being investigated as potential points of therapeutic intervention to block pathological EV signaling (Williams et al., 2019). Therapeutic strategies often focus on inhibiting these specific uptake routes to prevent the delivery of oncogenic or pro-inflammatory cargo. Understanding the specificity of these pathways is essential for developing targeted drug delivery systems that utilize EVs as natural nanocarriers.
Inhibition of vesicle-cell surface binding or disruption of endocytic internalization pathways (e.g., macropinocytosis, clathrin-mediated endocytosis).
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