ArticleFrontiers in cellular neuroscience2019
Comprehensive Evaluation of White Matter Damage and Neuron Death and Whole-Transcriptome Analysis of Rats With Chronic Cerebral Hypoperfusion.
Article in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- The Mechanism of Ferroptosis and Blood-Brain Barrier Damage in Cerebrovascular Diseases.Biomedicines · 2026Review
- Targeting Nurr1 With Amodiaquine Preserves Dendritic Spines and Cognitive Function After Chronic Cerebral Hypoperfusion.Neural plasticity · 2026Article
- Article
- Beyond Pharmacology: The Biological Mechanisms of Remote Ischemic Conditioning in Cerebrovascular Disease.Biomolecules · 2024Review
- Integrated Analysis of Chromatin and Transcriptomic Profiling Identifies PU.1 as a Core Regulatory Factor in Microglial Activation Induced by Chronic Cerebral Hypoperfusion.Molecular neurobiology · 2024Article
- Role of long non-coding RNAs in the pathophysiology of Alzheimer's disease and other dementias.Molecular biology reports · 2024Review
- A circRNA ceRNA network involved in cognitive dysfunction after chronic cerebral hypoperfusion.Aging · 2024Article
- VEGF Modulates the Neural Dynamics of Hippocampal Subregions in Chronic Global Cerebral Ischemia Rats.Neuromolecular medicine · 2021Article
- Impaired Cognitive Flexibility Induced by Chronic Cerebral Hypoperfusion in the 5XFAD Transgenic Mouse Model of Mixed Dementia.The journals of gerontology. Series A, Biological sciences and medical sciences · 2021Article
- Dl-3-n-Butylphthalide Alleviates Hippocampal Neuron Damage in Chronic Cerebral HypoperfusionFrontiers in aging neuroscience · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimsChronic cerebral hypoperfusion (CCH) is induced by chronic deficit of brain perfusion, contributes to a persistent or progressive cognitive dysfunction, which is characterized by diverse neuropathological manifestations. There are currently no effective medications available. White matter damage (WMD) and cortical neuron death may be caused by CCH, which are related to cognitive impairment, while the underlying molecular mechanisms remain unclear. In the study, a database of the transcriptome level was built to determine potential biomarkers in cortex of CCH.
methodsCCH was induced in male Sprague-Dawley rats by permanent occlusion of the bilateral common carotid arteries. Rats were randomly divided into three groups: Sham-operated group (
resultsCompared to the sham group, cognitive impairment, disintegration of white matter, blood-brain barrier damage and neuron death were induced by CCH. Neuron death including apoptosis and necroptosis might occur in the cortex of CCH. We constructed the regulatory networks of whole-transcriptomic including differentially expressed mRNAs, circRNAs, and lncRNAs, and related biological functions and pathways involved in neurological disease, cell death and survival, energy and metabolism, et al. Our results also indicated that Cyr61 mRNA may play a role in the CCH-related cortical neuronal death.
conclusionWMD and cortical neuronal death are worthy of attention in the pathogenesis of CCH. Additionally, the present results provide potential evidence at the whole-transcription level for CCH, offering candidate biomarkers and therapeutic targets.
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