Abstract—Recently, there have been a growing number of studies on the role of extracellular vesicles (EV) in brain functioning in health and disease. Signaling with the participation of astrocytic EVs under normal conditions and after ischemia is now mainly elucidated. In general, the stimuli that induce secretion of EVs from astrocytes, EV composition and the mechanism of EV binding to neurons are already known. It was shown that normal, non-pathological astrocytes secrete EVs, which suppress neuronal death after ischemia, resist oxidative stress, and promote plastic changes in neurons. Astrocytes in a pro-inflammatory environment secrete EVs which further enhance inflammation, neuronal death, and suppression of plastic rearrangements in neurons after ischemia. The review summarizes the latest results on the role of astrocytic EVs in the functioning of neurons and attempts to generalize the results.
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The study was supported by a grant from the Russian Science Foundation (project no. 21-75-20112).
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Abbreviations: AMPK, AMP-activated protein kinase; Atg7, an autophagy-associated protein 7; BDNF, brain-derived neurotrophic factor; GDNF, glial cell-derived neurotrophic factor; L1CAM, protein L1; mTOR, mammalian target of rapamycin; NCAM, neuronal cell adhesion molecule; PrP, prion protein; TNF alpha, tumor necrosis factor alpha; EV, extracellular vesicles.
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Yakovlev, A.A. Neuroprotective Effects of Astrocyte Extracellular Vesicles in Stroke. Neurochem. J. 16, 121–129 (2022). https://doi.org/10.1134/S1819712422020143
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DOI: https://doi.org/10.1134/S1819712422020143