期刊
NEUROLOGICAL RESEARCH
卷 28, 期 4, 页码 399-414出版社
TAYLOR & FRANCIS LTD
DOI: 10.1179/016164106X115008
关键词
subarachnoid hemorrhage; brain injury; signaling pathways; early vasospasm
资金
- NICHD NIH HHS [HD43120] Funding Source: Medline
- NINDS NIH HHS [NS43338, NS45694] Funding Source: Medline
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R01HD043120] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS045694, R01NS043338] Funding Source: NIH RePORTER
Objectives: Increasing body of experimental and clinical data indicates that early brain injury after initial bleeding largely contributes to unfavorable outcome after subarachnoid hemorrhage (SAH). This review presents molecular mechanisms underlying brain injury at its early stages after SAH. Methods: PubMed was searched using term 'subarachnoid hemorrhage' and key words referring to molecular and cellular pathomechanisms of SAH-induced early brain injury. Results: The authors reviewed intracranial phenomena and molecular agents that contribute to the early development of pathological sequelae of SAH in cerebral and vascular tissues, including cerebral ischemia and its interactions with injurious blood components, blood-brain barrier disruption, brain edema and apoptosis. Discussion: It is believed that detailed knowledge of molecular signaling pathways after SAH will serve to improve therapeutic interventions. The most promising approach is the protection of neurovascular unit including anti-apoptosis therapy.
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