ArticleACS chemical neuroscience2024
Increased Expression of VCAM1 on Brain Endothelial Cells Drives Blood-Brain Barrier Impairment Following Chronic Cerebral Hypoperfusion.
Article in ACS chemical neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Novel cell markers with altered expression in brain aging and Alzheimer's disease: A review.IBRO neuroscience reports · 2026Article
- Novel multi-omic biomarkers to combat oocyte and ovarian aging.GeroScience · 2026Article
- Neurovascular Unit Dysfunction and Neural Barrier Pathology in Dysautonomia: Molecular Links to Cardiovascular Autonomic Failure.International journal of molecular sciences · 2026Review
- Neuromodulation Techniques in Chronic Cerebral Hypoperfusion: Mechanisms and Therapeutic Advances.CNS neuroscience & therapeutics · 2026Review
- Neuroprotective effects of piracetam in vascular dementia: a review of toll-like receptor 4 -mediated neuroinflammatory pathways.Inflammopharmacology · 2026Review
- Exploring the Expression Changes of Immune Genes in Alzheimer's Disease: A Study on ANXA1, VCAM1, and CCL2.Molecular neurobiology · 2026Article
- APOE4 Alters Early Transcriptional Programs and Inflammatory Signaling in Human Induced Pluripotent Stem Cells.International journal of molecular sciences · 2026Article
- Review
- Targeting microglial C1q alleviates blood-brain barrier disruption in the thalamus after cortical infarction.Journal of neuroinflammation · 2026Article
- Simvastatin Ameliorates Lipid Metabolism-Mediated Endothelial Inflammation and Tight Junction Impairment in Chronic Cerebral Hypoperfusion.Neuromolecular medicine · 2026Article
- The effects of alcohol dependence on the CSF proteome in mice: Evidence for blood-brain barrier dysfunction and neuroinflammation.Neurobiology of disease · 2026Article
- The multi-target protective effects of quercetin in cerebrovascular diseases: a dietary strategy for endothelial repair and neuroprotection.Frontiers in nutrition · 2026Review
- Scaffold-free 3D-cell co-culture model system for the study of metastatic cancer in the brain TME.PloS one · 2026Article
- Single-cell transcriptomic analysis reveals age-related remodeling of brain endothelial cells.Aging brain · 2026Article
- Article
- The effects of Alcohol Dependence on the CSF Proteome in Mice: Evidence for Blood-Brain Barrier Dysfunction and Neuroinflammation.bioRxiv : the preprint server for biology · 2025Article
- Scaffold-free 3D-Cell Co-Culture Model System for the Study of Metastatic Cancer Cell Behavior in the Brain TME.bioRxiv : the preprint server for biology · 2025Article
- Impacts of systemic milieu on cerebrovascular and brain aging: insights from heterochronic parabiosis, blood exchange, and plasma transfer experiments.GeroScience · 2025Review
- Endothelial mitochondria in the blood-brain barrier.Fluids and barriers of the CNS · 2025Review
- Cerebrovascular p16Acta neuropathologica communications · 2025Article
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Authors and funding
5 authors.
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Abstract
Chronic cerebral hypoperfusion (CCH)-triggered blood-brain barrier (BBB) dysfunction is a core pathological change occurring in vascular dementia (VD). Despite the recent advances in the exploration of the structural basis of BBB impairment and the routes of entry of harmful compounds after a BBB leakage, the molecular mechanisms inducing BBB impairment remain largely unknown in terms of VD. Here, we employed a CCH-induced VD model and discovered increased vascular cell adhesion molecule 1 (VCAM1) expression on the brain endothelial cells (ECs). The expression of VCAM1 was directly correlated with the severity of BBB impairment. Moreover, the VCAM1 expression was associated with different regional white matter lesions. Furthermore, a compound that could block VCAM1 activation, K-7174, was also found to alleviate BBB leakage and protect the white matter integrity, whereas pharmacological manipulation of the BBB leakage did not affect the VCAM1 expression. Thus, our results demonstrated that VCAM1 is an important regulator that leads to BBB dysfunction following CCH. Blocking VCAM1-mediated BBB impairment may thus offer a new strategy to treat CCH-related neurodegenerative diseases.
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