Blood-Brain Barrier Disruption: A Common Driver of Central Nervous System Diseases

被引:25
|
作者
Segura-Collar, Berta [1 ]
Mata-Martinez, Pablo [1 ]
Hernandez-Lain, Aurelio [2 ]
Sanchez-Gomez, Pilar [1 ]
Gargini, Ricardo [1 ]
机构
[1] Inst Salud Carlos III UFIEC, Neurooncol Unit, Madrid, Spain
[2] Inst Invest Biomed I 12, Madrid, Spain
关键词
blood-brain barrier (BBB); neurovascular unit (NVU); pericytes; neurodegeneration; glioma; Alzheimer's disease; ASTROCYTE-ENDOTHELIAL INTERACTIONS; ALZHEIMERS-DISEASE; CEREBROVASCULAR INTEGRITY; MOLECULAR-MECHANISMS; NEUROVASCULAR UNIT; TUMOR VESSELS; PERICYTES; GLIOBLASTOMA; PHYSIOLOGY; ANGIOGENESIS;
D O I
10.1177/1073858420985838
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The brain is endowed with a unique cellular composition and organization, embedded within a vascular network and isolated from the circulating blood by a specialized frontier, the so-called blood-brain barrier (BBB), which is necessary for its proper function. Recent reports have shown that increments in the permeability of the blood vessels facilitates the entry of toxic components and immune cells to the brain parenchyma and alters the phenotype of the supporting astrocytes. All of these might contribute to the progression of different pathologies such as brain cancers or neurodegenerative diseases. Although it is well known that BBB breakdown occurs due to pericyte malfunctioning or to the lack of stability of the blood vessels, its participation in the diverse neural diseases needs further elucidation. This review summarizes what it is known about BBB structure and function and how its instability might trigger or promote neuronal degeneration and glioma progression, with a special focus on the role of pericytes as key modulators of the vasculature. Moreover, we will discuss some recent reports that highlights the participation of the BBB alterations in glioma growth. This pan-disease analysis might shed some light into these otherwise untreatable diseases and help to design better therapeutic approaches.
引用
收藏
页码:222 / 237
页数:16
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