ArticleImmunity, inflammation and disease2024
Downregulation of Notch Signaling-Stimulated Genes in Neurovascular Unit Alterations Induced by Chronic Cerebral Hypoperfusion.
Article in Immunity, inflammation and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Neuromodulation Techniques in Chronic Cerebral Hypoperfusion: Mechanisms and Therapeutic Advances.CNS neuroscience & therapeutics · 2026Review
- Roles of Microglia in Cerebral Small Vessel Disease.CNS neuroscience & therapeutics · 2026Review
- Capillary-Associated Microglia in Neurovascular Coupling: Localization, Mechanisms, and Disease Implications.Journal of neuroinflammation · 2026Review
- The association between obstructive sleep apnea and total cerebral small vessel disease burden-Neurovascular insights of OSA.Frontiers in neuroscience · 2026Article
- Temporal Evolution of Brain Inflammation in the Bilateral Common Carotid Artery Stenosis Model of Chronic Cerebral Hypoperfusion.Journal of inflammation research · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
backgroundChronic cerebral hypoperfusion (CCH) is a key contributor to vascular cognitive impairment (VCI) and is typically associated with blood-brain barrier (BBB) damage. This study investigates the pathological mechanisms underlying CCH-induced neurovascular unit (NVU) alterations.
methodsA mouse model of CCH was established using the bilateral common carotid artery stenosis (BCAS) procedure. Decreased cerebral blood flow (CBF) and impaired BBB integrity were assessed. Brain microvessel (BMV)-specific transcriptome profiles were analyzed using RNA-seq, supplemented with published single-cell RNA-seq data.
resultsRNA-seq revealed neuroinflammation-related gene activation and significant downregulation of Notch signaling pathway genes in BMVs post-BCAS. Upregulated differentially expressed genes (DEGs) were enriched in microglia/macrophages, while downregulated DEGs were prominent in endothelial cells and pericytes. Enhanced activation of vascular-associated microglia (VAM) was linked to neurovascular alterations.
conclusionCCH induces significant NVU changes, marked by microglia-associated neuroinflammation and Notch signaling downregulation. These insights highlight potential therapeutic targets for treating neuroinflammatory and vascular-related neurodegenerative diseases.
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Registered trials
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