ArticleInternational journal of molecular sciences2020
Role of HMGB1 in an Animal Model of Vascular Cognitive Impairment Induced by Chronic Cerebral Hypoperfusion.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Chronic cerebral hypoperfusion exacerbates amyloid and tau pathology by impairing glymphatic transport via AQP4- and VEGF-mediated pathways: insights from a vascular to mixed-type dementia model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- The Bidirectional Role of Hypoxia-Inducible Factor 1 Alpha in Vascular Dementia Caused by Chronic Cerebral Hypoperfusion.Molecular neurobiology · 2025Review
- Single-nucleus RNA sequencing of human periventricular white matter in vascular dementia.bioRxiv : the preprint server for biology · 2024Article
- Shared Proteins and Pathways of Cardiovascular and Cognitive Diseases: Relation to Vascular Cognitive Impairment.Journal of proteome research · 2024Article
- A circRNA ceRNA network involved in cognitive dysfunction after chronic cerebral hypoperfusion.Aging · 2024Article
- Assessing the Role of VISTA in Vascular Cognitive Impairment: Addressing Limitations and Exploring Future Research Directions [Letter].Clinical interventions in aging · 2024Article
- Heart-brain interaction in cardiogenic dementia: pathophysiology and therapeutic potential.Frontiers in cardiovascular medicine · 2024Review
- Update on the mechanism of microglia involvement in post-stroke cognitive impairment.Frontiers in aging neuroscience · 2024Review
- Hybrid surgery can improve neurocognitive function in patients with internal carotid artery occlusion.Scientific reports · 2023Article
- The correlation between the severity of cerebral microbleeds and serum HMGB1 levels and cognitive impairment in patients with cerebral small vessel disease.Frontiers in aging neuroscience · 2023Article
- Hemodynamic changes and neuronal damage detected by 9.4 T MRI in rats with chronic cerebral ischemia and cognitive impairment.Brain and behavior · 2022Article
- SP1 Promotes HDAC4 Expression and Inhibits HMGB1 Expression to Reduce Intestinal Barrier Dysfunction, Oxidative Stress, and Inflammatory Response after Sepsis.Journal of innate immunity · 2022Article
- Capsaicin Ameliorates the Loosening of Mitochondria-Associated Endoplasmic Reticulum Membranes and Improves Cognitive Function in Rats With Chronic Cerebral Hypoperfusion.Frontiers in cellular neuroscience · 2022Article
- HDACi protects against vascular cognitive impairment from CCH injury via induction of BDNF-related AMPA receptor activation.Journal of cellular and molecular medicine · 2021Article
- Higher level of acute serum VEGF and larger infarct volume are more frequently associated with post-stroke cognitive impairment.PloS one · 2020Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
The pathophysiology of vascular cognitive impairment (VCI) is associated with chronic cerebral hypoperfusion (CCH). Increased high-mobility group box protein 1 (HMGB1), a nonhistone protein involved in injury and inflammation, has been established in the acute phase of CCH. However, the role of HMGB1 in the chronic phase of CCH remains unclear. We developed a novel animal model of CCH with a modified bilateral common carotid artery occlusion (BCCAO) in C57BL/6 mice. Cerebral blood flow (CBF) reduction, the expression of HMGB1 and its proinflammatory cytokines (tumor necrosis factor-alpha [TNF-α], interleukin [IL]-1β, and IL-6), and brain pathology were assessed. Furthermore, we evaluated the effect of HMGB1 suppression through bilateral intrahippocampus injection with the CRISPR/Cas9 knockout plasmid. Three months after CCH induction, CBF decreased to 30-50% with significant cognitive decline in BCCAO mice. The 7T-aMRI showed hippocampal atrophy, but amyloid positron imaging tomography showed nonsignificant amyloid-beta accumulation. Increased levels of HMGB1, TNF-α, IL-1β, and IL-6 were observed 3 months after BCCAO. HMGB1 suppression with CRISPR/Cas9 knockout plasmid restored TNF-α, IL-1β, and IL-6 and attenuated hippocampal atrophy and cognitive decline. We believe that HMGB1 plays a pivotal role in CCH-induced VCI pathophysiology and can be a potential therapeutic target of VCI.
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