Blood-brain barrier dysfunction following traumatic brain injury

被引:116
作者
Alluri, Himakarnika [1 ,2 ]
Wiggins-Dohlvik, Katie [1 ,2 ]
Davis, Matthew L. [1 ,2 ]
Huang, Jason H. [2 ,3 ]
Tharakan, Binu [1 ,2 ]
机构
[1] Baylor Scott & White Hlth, Dept Surg, Temple, TX 76504 USA
[2] Texas A&M Univ, Hlth Sci Ctr, Coll Med, Temple, TX 76504 USA
[3] Baylor Scott & White Hlth, Dept Neurosurg, Temple, TX 76504 USA
关键词
Blood-brain barrier; Traumatic brain injury; Central nervous system trauma; Vascular permeability; Brain edema; CEREBRAL EDEMA; CELLULAR EDEMA; UNITED-STATES; CNS INJURY; RAT MODEL; T-CELLS; PATHOPHYSIOLOGY; DISRUPTION; PERMEABILITY; EXPRESSION;
D O I
10.1007/s11011-015-9651-7
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Traumatic brain injury is a serious cause of morbidity and mortality worldwide. After traumatic brain injury, the blood-brain barrier, the protective barrier between the brain and the intravascular compartment, becomes dysfunctional, leading to leakage of proteins, fluid, and transmigration of immune cells. As this leakage has profound clinical implications, including edema formation, elevated intracranial pressure and decreased perfusion pressure, much interest has been paid to better understanding the mechanisms responsible for these events. Various molecular pathways and numerous mediators have been found to be involved in the intricate process of regulating blood-brain barrier permeability following traumatic brain injury. This review provides an update to the existing knowledge about the various pathophysiological pathways and advancements in the field of blood-brain barrier dysfunction and hyperpermeability following traumatic brain injury, including the role of various tight junction proteins involved in blood-brain barrier integrity and regulation. We also address pitfalls of existing systems and propose strategies to improve the various debilitating functional deficits caused by this progressive epidemic.
引用
收藏
页码:1093 / 1104
页数:12
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