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The review analyzes the role of extracellular vesicles (EVs)—nanoparticles secreted by all cells (endothelium, neurons, glia, and blood cells) in the development of ischemic stroke (IS). EVs transport proteins, lipids, microRNAs, and other "cargoes," serving as a means of intercellular communication. In IS, the cells of the neurovascular unit and blood cells change their EV secretion profile. These EVs are involved in the initiation and maintenance of pathological processes: endothelial dysfunction, proinflammatory activation, apoptosis, disruption of the blood-brain barrier, and hypercoagulability. In clinical studies circulating EVs levels and composition, as well as vesicle-born microRNAs, correlate with the presence, severity, and volume of infarction and prognosis of ischemic stroke, offering promising tools for early diagnosis and monitoring. Experimental studies have shown that EVs of some cells (astrocytes, mesenchymal stem cells) have neuroprotective properties, transferring protective molecules and mitochondria to damaged neurons. The creation of engineered EVs loaded with therapeutic molecules (microRNA, neurotrophic factors, etc.) or mitochondria opens new possibilities for the development of targeted neuroprotective and reparative stroke therapy.
Keywords:ischemic stroke, extracellular vesicles, stroke markers, neuroprotection, mitochondria transfer, microRNA, targeted therapies for ischemic stroke.
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