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Prog Neurobiol. 2018 Apr - May;163-164:144-171. doi: 10.1016/j.pneurobio.2017.10.001. Epub 2017 Oct 5.

Blood-brain barrier dysfunction and recovery after ischemic stroke.

Author information

1
Pittsburgh Institute of Brain Disorders & Recovery and Department of Neurology, University of Pittsburgh, Pittsburgh, PA 15213, USA; State Key Laboratory of Medical Neurobiology, Institute of Brain Sciences and Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China.
2
Department of Neurosurgery, University of Michigan, Ann Arbor, MI 48109, USA.
3
Pittsburgh Institute of Brain Disorders & Recovery and Department of Neurology, University of Pittsburgh, Pittsburgh, PA 15213, USA.
4
State Key Laboratory of Medical Neurobiology, Institute of Brain Sciences and Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China; Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
5
Department of Neurosurgery, University of Michigan, Ann Arbor, MI 48109, USA. Electronic address: rkeep@umich.edu.
6
Pittsburgh Institute of Brain Disorders & Recovery and Department of Neurology, University of Pittsburgh, Pittsburgh, PA 15213, USA. Electronic address: shiy3@upmc.edu.

Abstract

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.

KEYWORDS:

Inflammation; Neurovascular unit; Repair; Stroke comorbidities; Tight junction

PMID:
28987927
PMCID:
PMC5886838
[Available on 2019-04-01]
DOI:
10.1016/j.pneurobio.2017.10.001
[Indexed for MEDLINE]

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