Research progress of mechanisms for tight junction damage on blood-brain barrier inflammation

被引:42
作者
Zhao, Bo [1 ]
Yin, Qiyang [1 ]
Fei, Yuxiang [1 ]
Zhu, Jianping [1 ]
Qiu, Yanying [1 ]
Fang, Weirong [1 ]
Li, Yunman [1 ]
机构
[1] China Pharmaceut Univ, Sch Basic Med & Clin Pharm, State Key Lab Nat Med, Nanjing 210009, Peoples R China
关键词
Blood-brain barrier; tight junction; inflammation; tight junction proteins; ADHESION MOLECULE-A; TOLL-LIKE RECEPTORS; ISCHEMIC-STROKE; THERAPEUTIC TARGETS; TRICELLULIN; PROTEINS; OCCLUDIN; DISRUPTION; EXPRESSION; MICROGLIA;
D O I
10.1080/13813455.2020.1784952
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
Inflammation in the central nervous system (CNS) contributes to disease pathologies by disrupting the integrity of the blood-brain barrier (BBB). Tight junctions (TJ) are a key component of the BBB. Following hypoxic-ischaemic or mechanical injury to the brain, inflammatory mediators are released such as cytokines, chemokines, and growth factors. Simultaneously, matrix metalloproteinases (MMPs) are released which can degrade TJ proteins. Subsequently, the function and morphology of the BBB are disrupted, which allows immune cells an opportunity to enter into the brain parenchyma. This review summarises the information on the role of TJ protein families in the BBB and provides a comprehensive summary of the mechanisms whereby inflammation breaks down the BBB by increasing degradation of TJ proteins.
引用
收藏
页码:1579 / 1590
页数:12
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