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Focusing on claudin-5: A promising candidate in the regulation of BBB to treat ischemic stroke
Abstract
Claudin-5 is a tight junction (TJ) protein in the blood-brain barrier (BBB) that has recently attracted increased attention. Numerous studies have demonstrated that claudin-5 regulates the integrity and permeability of the BBB. Increased claudin-5 expression plays a neuroprotective role in neurological diseases, particularly in cerebral ischemic stroke. Moreover, claudin-5 might be a potential marker for early hemorrhagic transformation detection in ischemic stroke. In light of the distinctive effects of claudin-5 on the nervous system, we present the elaborate network of roles that claudin-5 plays in ischemic stroke. In this review, we first introduce basic knowledge regarding the BBB and the claudin family, the characterization and regulation of claudin-5, and association between claudin-5 and other TJ proteins. Subsequently, we describe BBB dysfunction and neuron-specific drivers of pathogenesis of ischemic stroke, including inflammatory disequilibrium and oxidative stress. Furthermore, we summarize promising ischemic stroke treatments that target the BBB via claudin-5, including modified rt-PA therapy, pharmacotherapy, hormone treatment, receptor-targeted therapy, gene therapy, and physical therapy. This review highlights recent advances and provides a comprehensive summary of claudin-5 in the regulation of the BBB and may be helpful for drug design and clinical therapy for treatment of ischemic stroke.
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“Astrocytic processes surround most of the vascular surface, regulating the blood–brain barrier (BBB) permeability [6, 7, 8, 9]—by modulating tight junction proteins such as claudin‐5 [10], or endothelial proteins such vimentin, which is associated with the stability of cerebral vasculature [11]—and integrate neuronal activity with blood flow [1, 2, 3, 4, 5, 12, 13, 14, 15, 16, 17, 18, 19, 20].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: APOE3 Christchurch homozygote glioprotection (2023) · cites this paper as [10]
In the citing paper
“claudin‐5 is crucial for the selective permeability of the BBB [10]”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: APOE3 Christchurch homozygote glioprotection (2023) · cites this paper as [10]
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Metadata
- Authors
- Lv, J., Hu, W., Yang, Z., Li, T., Jiang, S., Ma, Z., Chen, F., & Yang, Y.
- Affiliations
- Northwest University (CN)
- Air Force Medical University (CN)
- Tang Du Hospital (CN)
- Corresponding author
- Yang, Yang
- Venue
- Progress in Neurobiology
- Publisher
- Elsevier BV
- Published
- 2018-02
- Volume
- 161
- Pages
- 79-96
- ISSN
- 0301-0082 (ISSN-L)
- OpenAlex
- W2771763619
- Cited by
- 148
- References
- 179
- Citations by year
- 2026: 7 · 2025: 17 · 2024: 16 · 2023: 13 · 2022: 17 · 2021: 26 · 2020: 23 · 2019: 16 · 2018: 13
- FWCI
- 1.37
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Progress in Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81500263)
- China Postdoctoral Science Foundation (2016T90973, 2015M572681)
- Topics
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Health Sciences › Medicine › Clinical Neurology › Acute Ischemic Stroke Management
- Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
- Keywords
- claudin-5, blood-brain barrier, ischemic stroke, tight junction proteins, blood-brain barrier permeability, hemorrhagic transformation, neuroprotection, oxidative stress, neuroinflammation, gene therapy, hormone therapy, receptor-targeted therapy, physiotherapy
- MeSH terms
- Animals, Blood-Brain Barrier, Brain Ischemia, Humans, Tissue Plasminogen Activator, Tight Junctions, Stroke, Claudin-5
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