Early Brain Injury Following Aneurysmal. Subarachnoid Hemorrhage: Emphasis on Cellular Apoptosis

被引:64
|
作者
Yuksel, Simge [2 ]
Tosun, Yusuf Berk [2 ]
Cahill, Julian [3 ]
Solaroglu, Ihsan [1 ]
机构
[1] Koc Univ, Fac Med, Dept Neurosurg, Istanbul, Turkey
[2] Koc Univ, Fac Med, Neurosci Res Lab, Istanbul, Turkey
[3] Univ Hosp Coventry & Warwickshire, Dept Neurosurg, Coventry, W Midlands, England
关键词
Apoptosis; Early brain injury; p53; Stroke; Subarachnoid hemorrhage; CEREBRAL VASOSPASM; ENDOTHELIAL-CELLS; CYTOCHROME-C; MODEL; DEATH; MITOCHONDRIA; MECHANISMS; CASPASES; MODULATION; ACTIVATION;
D O I
10.5137/1019-5149.JTN.5731-12.1
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Subarachnoid hemorrhage (SAH) due to intracranial aneurysm rupture is a complex clinical disease with high mortality and morbidity. Recent studies suggest that early brain injury (EBI) rather than vasospasm might be responsible for morbidity and mortality within 24-72 hours after SAH. The rise in intracranial pressure following SAH causes a significant drop in cerebral perfusion press re that leads to global cerebral ischemia and initiates the acute injury cascade. Various molecular mechanisms have been shown to involve in the pathophysiology of EBI including cellular apoptosis. In this review, we summarize apoptotic molecular mechanisms involved in the etiology of EBI and its potential as a target for future therapeutic intervention.
引用
收藏
页码:529 / 533
页数:5
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