Astrocyte-Derived Extracellular Vesicles for Ischemic Stroke: Therapeutic Potential and Prospective

Stroke is a leading cause of death and disability in the world. Astrocytes are special glial cells within the central nervous system and play important roles in mediating neuroprotection and repair processes during stroke. Extracellular vesicles (EVs) are lipid bilayer particles released from cells...

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Bibliographic Details
Published in:Aging and disease 2024-06, Vol.15 (3), p.1227-1254
Main Authors: Wang, Xianghui, Li, Aihua, Fan, Huaju, Li, Yanyan, Yang, Nana, Tang, Yaohui
Format: Article
Language:English
Subjects:
Amino acids
Animals
Astrocytes
Astrocytes - metabolism
Astrocytes - pathology
Care and treatment
Cell organelles
Extracellular Vesicles - metabolism
Extracellular Vesicles - transplantation
Health aspects
Humans
Ischemia
Ischemic Stroke - metabolism
Ischemic Stroke - pathology
Ischemic Stroke - therapy
Membrane lipids
Physiological aspects
Proteins
Review
RNA
Stroke (Disease)
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Summary:Stroke is a leading cause of death and disability in the world. Astrocytes are special glial cells within the central nervous system and play important roles in mediating neuroprotection and repair processes during stroke. Extracellular vesicles (EVs) are lipid bilayer particles released from cells that facilitate intercellular communication in stroke by delivering proteins, lipids, and RNA to target cells. Recently, accumulating evidence suggested that astrocyte-derived EVs (ADEVs) are actively involved in mediating numerous biological processes including neuroprotection and neurorepair in stroke and they are realized as an excellent therapeutic approach for treating stroke. In this review we systematically summarize the up-to-date research on ADEVs in stroke, and prospects for its potential as a novel therapeutic target for stroke. We also provide an overview of the effects and functions of ADEVs on stroke recovery, which may lead to developing clinically relevant therapies for stroke.
ISSN:2152-5250
2152-5250
DOI:10.14336/AD.2023.0823-1