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Cell-surface adhesion and uptake receptors for platelet-derived extracellular vesicles (PEVs) are a diverse set of proteins on recipient cells, such as endothelial cells and leukocytes, that mediate the binding and internalization of PEVs. PEVs, also known as platelet microparticles, are the most abundant extracellular vesicles in human blood and carry a variety of bioactive molecules, including proteins, lipids, and RNAs, which they deliver to target cells to modulate their function. Adhesion is typically initiated by the interaction between P-selectin on the PEV surface and P-selectin glycoprotein ligand-1 (PSGL-1) on the recipient cell. Subsequent uptake is often mediated by receptors that recognize phosphatidylserine (PS) exposed on the PEV membrane, such as the scavenger receptor CD36 and the TAM receptor family (Axl, MerTK). These receptors play significant roles in thrombo-inflammation, vascular homeostasis, and cancer progression. Therapeutic strategies targeting these receptors or their ligands, such as the P-selectin inhibitor crizanlizumab or Axl inhibitors like bemcentinib, are being investigated for their potential to treat cardiovascular and inflammatory disorders by disrupting PEV-mediated pathological signaling.
Inhibition of receptor-ligand interactions between platelet-derived extracellular vesicles and recipient cells, such as blocking P-selectin/PSGL-1 adhesion or phosphatidylserine-mediated uptake.
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