ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2022
Nox2 underpins microvascular inflammation and vascular contributions to cognitive decline.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 9 citations in OpenAlex.
- Gene expression and brain pathology at the early stages of bilateral chronic cerebral hypoperfusion in the female mouse brain.Experimental neurology · 2026Article
- Compartmentalized B cell-microglia crosstalk drives ischemic white matter demyelination.Nature communications · 2026Article
- Hydrogen sulfide mitigates spatial learning deficits in angiotensin II-Induced hypertension via inhibition of endothelial NOX2 and neuroinflammation.Translational psychiatry · 2026Article
- Transcriptomic Evidence of MAS1 Receptor Dysregulation and a Failed Compensatory State in Human Vascular Cognitive Impairment.medRxiv : the preprint server for health sciences · 2026Article
- Redox Regulation of Microvascular Physiology and Pathophysiology: Insights into Therapeutic Strategies and Limitations.Antioxidants & redox signaling · 2025Review
- Lack of intracranial atherosclerosis in various atherosclerotic mouse models.Vascular biology (Bristol, England) · 2025Article
- Necroptosis in vascular cognitive impairment: mechanisms and therapeutic potential.Frontiers in aging neuroscience · 2025Review
- The relationship of neuropsychiatric symptoms with inflammatory markers in the hippocampus and cingulate cortex of bipolar disorder subjects: A post-mortem study.Journal of psychiatric research · 2024Article
- NOX-induced oxidative stress is a primary trigger of major neurodegenerative disorders.Progress in neurobiology · 2023Review
- Recent advances in mechanistic, therapeutic, and diagnostic research of cerebrovascular diseases: updates from brain & BrainPET 2022.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- CRTC1 is a potential target to delay aging-induced cognitive deficit by protecting the integrity of the blood-brain barrier via inhibiting inflammation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Review
- Effects of linalyl acetate on oxidative stress, inflammation and endothelial dysfunction: can linalyl acetate prevent mild cognitive impairment?Frontiers in pharmacology · 2023Review
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
Chronic microvascular inflammation and oxidative stress are inter-related mechanisms underpinning white matter disease and vascular cognitive impairment (VCI). A proposed mediator is nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (Nox2), a major source of reactive oxygen species (ROS) in the brain. To assess the role of Nox2 in VCI, we studied a tractable model with white matter pathology and cognitive impairment induced by bilateral carotid artery stenosis (BCAS). Mice with genetic deletion of Nox2 (Nox2 KO) were compared to wild-type (WT) following BCAS. Sustained BCAS over 12 weeks in WT mice induced Nox2 expression, indices of microvascular inflammation and oxidative damage, along with white matter pathology culminating in a marked cognitive impairment, which were all protected by Nox2 genetic deletion. Neurovascular coupling was impaired in WT mice post-BCAS and restored in Nox2 KO mice. Increased vascular expression of chemoattractant mediators, cell-adhesion molecules and endothelial activation factors in WT mice post-BCAS were ameliorated by Nox2 deficiency. The clinical relevance was confirmed by increased vascular Nox2 and indices of microvascular inflammation in human post-mortem subjects with cerebral vascular disease. Our results support Nox2 activity as a critical determinant of VCI, whose targeting may be of therapeutic benefit in cerebral vascular disease.
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