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- W2917788843 abstract "Aneurysmal subarachnoid hemorrhage remains serious hemorrhagic stroke with high morbidities and mortalities. Aneurysm rupture causes arterial bleeding-induced mechanical brain tissue injuries and elevated intracranial pressure, followed by global cerebral ischemia. Post-subarachnoid hemorrhage ischemia, tissue injuries as well as extravasated blood components and the breakdown products activate microglia, astrocytes and Toll-like receptor 4, and disrupt blood-brain barrier associated with the induction of many inflammatory and other cascades. Once blood-brain barrier is disrupted, brain tissues are directly exposed to harmful blood contents and immune cells, which aggravate brain injuries furthermore. Blood-brain barrier disruption after subarachnoid hemorrhage may be developed by a variety of mechanisms including endothelial cell apoptosis and disruption of tight junction proteins. Many molecules and pathways have been reported to disrupt the blood-brain barrier after subarachnoid hemorrhage, but the exact mechanisms remain unclear. Multiple independent and/or interconnected signaling pathways may be involved in blood-brain barrier disruption after subarachnoid hemorrhage. This review provides recent understandings of the mechanisms and the potential therapeutic targets of blood-brain barrier disruption after subarachnoid hemorrhage." @default.
- W2917788843 created "2019-03-02" @default.
- W2917788843 creator A5021894952 @default.
- W2917788843 creator A5046362015 @default.
- W2917788843 date "2019-01-01" @default.
- W2917788843 modified "2023-10-16" @default.
- W2917788843 title "Potential therapeutic molecular targets for blood-brain barrier disruption after subarachnoid hemorrhage" @default.
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- W2917788843 doi "https://doi.org/10.4103/1673-5374.251190" @default.
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