Blood-brain barrier dysfunction and recovery after ischemic stroke

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.

Increased blood-brain barrier permeability in contralateral hemisphere predicts worse outcome in acute ischemic stroke after reperfusion therapy

“…The increased BBBP in the mirror lesion region may be a result of hemispheric diaschisis, induced by the ischemic region via transcallosal commissure fibers. As we mentioned earlier, stroke risk factors, such as hypertension, diabetes, hyperlipidemia, ageing, and sex, have an effect on BBBP, and they even exacerbate BBB disruption after stroke 27. It is possible that the disruption of BBBP in AIS is superimposed on chronic diffuse dysfunction of BBB.…”

SALM4 regulates angiogenic functions in endothelial cells through VEGFR2 phosphorylation at Tyr1175

“…The current treatment for acute ischemia is largely dependent on tissue plasminogen activator-mediated thrombolysis. However, this treatment exacerbates the risk of hemorrhage, which is related to BBB breakdown (56). Because BBB stabilization increases the efficacy of tissue plasminogen activator treatment, BBB stabilization is critical for reducing poor outcomes in patients with acute ischemia.…”

Total Glycosides of Cistanche deserticola Promote Neurological Function Recovery by Inducing Neurovascular Regeneration via Nrf-2/Keap-1 Pathway in MCAO/R Rats

“…BBB disruption can elevate brain water content and tissue swelling, leading to brain injury. Tight junction proteins are important structural components of the BBB (Tenreiro et al, 2016;Jiang et al, 2018). To test whether TGs, PSs, and OSs treatment after stroke might influence BBB integrity, the expressions of ZO-1, claudin-5, and occludin were performed by immunofluorescence analysis.…”