Different roles of astrocytes in the blood-brain barrier during the acute and recovery phases of stroke

Ischemic stroke, a frequently occurring form of stroke, is caused by obstruction of cerebral blood flow, which leads to ischemia, hypoxia, and necrosis of local brain tissue. After ischemic stroke, both astrocytes and the blood-brain barrier undergo morphological and functional transformations. Howe...

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Vydané v:Neural regeneration research Ročník 21; číslo 4; s. 1359 - 1372
Hlavní autori: Cheng, Jialin, Zheng, Yuxiao, Cheng, Fafeng, Wang, Chunyu, Han, Jinhua, Zhang, Haojia, Lan, Xin, Zhang, Chuxin, Wang, Xueqian, Wang, Qingguo, Li, Changxiang
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: India Wolters Kluwer - Medknow 01.04.2026
Medknow Publications & Media Pvt. Ltd
Wolters Kluwer Medknow Publications
Vydanie:2
Predmet:
astrocytes
axon
Blood-brain barrier
cytokines
endothelial cells
glial scar
Growth factors
Ischemia
ischemic stroke
Morphology
phenotype
remodel
Review
vascular
blood-brain barrier
phenotype
endothelial cells
glial scar
remodel
cytokines
astrocytes
axon
vascular
ischemic stroke
blood–brain barrier
ISSN:1673-5374, 1876-7958
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Shrnutí:Ischemic stroke, a frequently occurring form of stroke, is caused by obstruction of cerebral blood flow, which leads to ischemia, hypoxia, and necrosis of local brain tissue. After ischemic stroke, both astrocytes and the blood-brain barrier undergo morphological and functional transformations. However, the interplay between astrocytes and the blood-brain barrier has received less attention. This comprehensive review explores the physiological and pathological morphological and functional changes in astrocytes and the blood-brain barrier in ischemic stroke. Post-stroke, the structure of endothelial cells and peripheral cells undergoes alterations, causing disruption of the blood-brain barrier. This disruption allows various pro-inflammatory factors and chemokines to cross the blood-brain barrier. Simultaneously, astrocytes swell and primarily adopt two phenotypic states: A1 and A2, which exhibit different roles at different stages of ischemic stroke. During the acute phase, A1 reactive astrocytes secrete vascular endothelial growth factor, matrix metalloproteinases, lipid carrier protein-2, and other cytokines, exacerbating damage to endothelial cells and tight junctions. Conversely, A2 reactive astrocytes produce pentraxin 3, Sonic hedgehog, angiopoietin-1, and other protective factors for endothelial cells. Furthermore, astrocytes indirectly influence blood-brain barrier permeability through ferroptosis and exosomes. In the middle and late (recovery) stages of ischemic stroke, A1 and A2 astrocytes show different effects on glial scar formation. A1 astrocytes promote glial scar formation and inhibit axon growth via glial fibrillary acidic protein, chondroitin sulfate proteoglycans, and transforming growth factor-β. In contrast, A2 astrocytes facilitate axon growth through platelet-derived growth factor, playing a crucial role in vascular remodeling. Therefore, enhancing our understanding of the pathological changes and interactions between astrocytes and the blood-brain barrier is a vital therapeutic target for preventing further brain damage in acute stroke. These insights may pave the way for innovative therapeutic strategies for ischemic stroke.
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ISSN:1673-5374
1876-7958
DOI:10.4103/NRR.NRR-D-24-01417