期刊
PROGRESS IN NEUROBIOLOGY
卷 163, 期 -, 页码 144-171出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pneurobio.2017.10.001
关键词
Inflammation; Neurovascular unit; Repair; Stroke comorbidities; Tight junction
资金
- U.S. National Institutes of Health [NS089534, NS045048, NS056118, NS036736, NS095029, NS098066, NS093399]
- U.S. Department of Veterans Affairs (VA) [BX002495]
- Chinese Natural Science Foundation [81529002]
- VA Senior Research Career Scientist Award
- Richard King Mellon Endowed Professorship
- University of Pittsburgh Medical Center (UPMC) Endowed Professorship
- State Administration of Foreign Experts Affairs, China [GDW20133100069]
- American Heart Association [15POST22260011]
- American Diabetes Association [1-16-IBS-008]
The blood-brain barrier (BBB) plays a vital role in regulating the trafficking of fluid, solutes and cells at the blood-brain interface and maintaining the homeostatic microenvironment of the CNS. Under pathological conditions, such as ischemic stroke, the BBB can be disrupted, followed by the extravasation of blood components into the brain and compromise of normal neuronal function. This article reviews recent advances in our knowledge of the mechanisms underlying BBB dysfunction and recovery after ischemic stroke. CNS cells in the neurovascular unit, as well as blood-borne peripheral cells constantly modulate the BBB and influence its breakdown and repair after ischemic stroke. The involvement of stroke risk factors and comorbid conditions further complicate the pathogenesis of neurovascular injury by predisposing the BBB to anatomical and functional changes that can exacerbate BBB dysfunction. Emphasis is also given to the process of long-term structural and functional restoration of the BBB after ischemic injury. With the development of novel research tools, future research on the BBB is likely to reveal promising potential therapeutic targets for protecting the BBB and improving patient outcome after ischemic stroke. (C) 2017 Elsevier Ltd. All rights reserved.
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