Mechanisms of Blood-Brain Barrier Dysfunction in Traumatic Brain Injury

被引:162
|
作者
Cash, Alison [1 ]
Theus, Michelle H. [1 ,2 ]
机构
[1] Virginia Maryland Coll Vet Med, Dept Biomed Sci & Pathobiol, Blacksburg, VA 24061 USA
[2] Virginia Maryland Coll Vet Med, Ctr Regenerat Med, Blacksburg, VA 24061 USA
基金
美国国家卫生研究院;
关键词
Blood-brain barrier disruption; TBI; endothelial cells; vascular-astrocyte coupling; aquaporin; edema; ASTROCYTE-ENDOTHELIAL INTERACTIONS; NECROSIS-FACTOR-ALPHA; DIFFUSION TENSOR; CEREBRAL MICROBLEEDS; ONCOSTATIN-M; AQUAPORIN; HEMORRHAGIC TRANSFORMATION; DECREASED EXPRESSION; MEDIATED DISRUPTION; ZONULA OCCLUDENS-1;
D O I
10.3390/ijms21093344
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Traumatic brain injuries (TBIs) account for the majority of injury-related deaths in the United States with roughly two million TBIs occurring annually. Due to the spectrum of severity and heterogeneity in TBIs, investigation into the secondary injury is necessary in order to formulate an effective treatment. A mechanical consequence of trauma involves dysregulation of the blood-brain barrier (BBB) which contributes to secondary injury and exposure of peripheral components to the brain parenchyma. Recent studies have shed light on the mechanisms of BBB breakdown in TBI including novel intracellular signaling and cell-cell interactions within the BBB niche. The current review provides an overview of the BBB, novel detection methods for disruption, and the cellular and molecular mechanisms implicated in regulating its stability following TBI.
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收藏
页数:27
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