Molecular pathophysiology of cerebral hemorrhage: secondary brain injury.
Molecular pathophysiology of cerebral hemorrhage: secondary brain injury.
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DOI：
10.1161/strokeaha.110.596718
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发表时间：
2011-06
期刊：
影响因子：
8.3
通讯作者：
Zhao X
中科院分区：
文献类型：
--
作者：
Aronowski J;Zhao X
脑出血(ICH)是一种经常致命的中风类型，在美国每年导致约30,000人死亡。如果患者在癫痫发作中幸存下来，脑实质内的血肿会触发一系列不良事件，导致二次侮辱和严重的神经功能障碍。本文讨论了脑出血后继发性脑损伤的某些方面，并概述了与血肿毒性、氧化应激和炎症相关的关键机制。最后，这篇综述讨论了血肿消退过程作为脑出血治疗靶点的相关性，并提出了潜在的临床相关分子靶点，可用于治疗与脑出血损伤相关的继发性损伤。
Intracerebral hemorrhage (ICH) is an often fatal type of stroke which kills about 30,000 people annually in the USA. If the patient survives the ictus, the resulting hematoma within brain parenchyma triggers a series of adverse events causing secondary insults and severe neurological deficits. This article discusses selected aspects of secondary brain injury after ICH and outlines key mechanisms associated with hematoma toxicity, oxidative stress, and inflammation. Finally, this review discusses the relevance of hematoma resolution processes as a target for ICH therapy, and presents potential clinically relevant molecular targets that could be harnessed to treat secondary injury associated with ICH injury.