Neuroinflammation and blood-brain barrier disruption following traumatic brain injury: Pathophysiology and potential therapeutic targets.
Neuroinflammation and blood-brain barrier disruption following traumatic brain injury: Pathophysiology and potential therapeutic targets.
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DOI：
10.1002/jnr.24331
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发表时间：
2020-01
影响因子：
4.2
通讯作者：
Huang JH
中科院分区：
文献类型：
--
作者：
Sulhan S;Lyon KA;Shapiro LA;Huang JH
创伤性脑损伤(TBI)是发达国家年轻人和儿童最常见的死亡和残疾原因，仅在美国就有170多万人死亡，造成5万人死亡。疾病控制和预防中心估计，美国有320万至530万人患有与脑外伤相关的残疾，包括几种神经认知障碍和功能限制。继颅脑损伤的原发机械性损伤后，文献表明存在延迟性继发性损伤，涉及各种神经炎性变化。在颅脑损伤后的几个小时到几天内，几个信号分子和代谢紊乱会导致血脑屏障(BBB)的破坏，导致免疫细胞外溢和脑水肿。颅脑损伤中的原发突发性损伤是撞击的直接结果，因此无法治疗，但延迟性继发性损伤的时间线和病理生理学为可能的治疗选择提供了一个窗口。本综述的目的是讨论颅脑损伤的原发和迟发性损伤的病理生理学，并介绍几项临床前研究，以确定潜在的治疗脑外伤的分子靶点。此外，还简要讨论了近期的某些临床试验，以说明脑外伤研究的现状。
Traumatic Brain Injury (TBI) is the most frequent cause of death and disability in young adults and children in the developed world, occurring in over 1.7 million persons and resulting in 50,000 deaths in the United States alone. The Centers for Disease Control and Prevention estimate that between 3.2 and 5.3 million persons in the United States live with a TBI-related disability, including several neurocognitive disorders and functional limitations. Following the primary mechanical injury in TBI, literature suggests the presence of a delayed secondary injury involving a variety of neuroinflammatory changes. In the hours to days following a TBI, several signaling molecules and metabolic derangements result in disruption of the blood-brain barrier (BBB), leading to an extravasation of immune cells and cerebral edema. The primary, sudden injury in TBI occurs as a direct result of impact and therefore cannot be treated, but the timeline and pathophysiology of the delayed, secondary injury allows for a window of possible therapeutic options. The goal of this review is to discuss the pathophysiology of the primary and delayed injury in TBI as well as present several preclinical studies that identify molecular targets in the potential treatment of TBI. Additionally, certain recent clinical trials are briefly discussed to demonstrate the current state of TBI investigation.
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DOI：
10.1136/bmj.d3795
发表时间：
2011-07-01
期刊：
BMJ (Clinical research ed.)
影响因子：
--
作者：
CRASH-2 Collaborators, Intracranial Bleeding Study
通讯作者：
CRASH-2 Collaborators, Intracranial Bleeding Study
影响因子：
2
作者：
Fakharian, Esmaeil;Abedzadeh-Kalahroudi, Masoumeh;Atoof, Fatemeh
通讯作者：
Atoof, Fatemeh
影响因子：
9.3
作者：
Colton CA;Mott RT;Sharpe H;Xu Q;Van Nostrand WE;Vitek MP
通讯作者：
Vitek MP
影响因子：
6.9
作者：
Chodobski A;Zink BJ;Szmydynger-Chodobska J
通讯作者：
Szmydynger-Chodobska J
影响因子：
64.8
作者：
Baker, Matt;Mackenzie, Ian R.;Hutton, Mike
通讯作者：
Hutton, Mike