Department of Neurosurgery, Georgia Health Sciences University, 1120 15th Street, Augusta, GA, 30912, USA.
Transl Stroke Res. 2011 Dec;2(4):633-42. doi: 10.1007/s12975-011-0129-6. Epub 2011 Nov 9.
Traumatic brain injury (TBI) remains a leading cause of mortality and morbidity worldwide. A major focus of preclinical research has focused on understanding the mechanisms of acute cell death after TBI; however, translation of these findings into the clinic has failed to improve long-term patient outcomes. Recent work suggests astrocytes, the predominant cell type within the human brain, may actively contribute to neurological demise by exacerbating secondary brain injury after TBI. Along these lines, astrocytes may promote neuroinflammation, increase the development of cerebral edema, and contribute to elevated intracranial pressure after brain injury. The primary goal of this mini-review is to summarize the growing body of literature that suggests reactive astrocytes influence the brain response to TBI. To maintain focus, we will limit our discussion to the mechanisms of cerebral edema.
创伤性脑损伤（TBI）仍然是全球范围内导致死亡和发病的主要原因。临床前研究的一个主要重点是了解 TBI 后急性细胞死亡的机制；然而，这些发现未能转化为临床，未能改善长期患者预后。最近的研究表明，星形胶质细胞是人类大脑中的主要细胞类型，可能通过加剧 TBI 后的继发性脑损伤，积极促进神经功能丧失。在这方面，星形胶质细胞可能会促进神经炎症，增加脑水肿的发展，并导致脑损伤后颅内压升高。本篇综述的主要目的是总结越来越多的文献，这些文献表明反应性星形胶质细胞影响大脑对 TBI 的反应。为了保持重点，我们将把讨论限制在脑水肿的机制上。
