ArticleNature communications2025
Chronic cerebral hypoperfusion induces venous dysfunction via EPAS1 regulation in mice.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Neuromodulation Techniques in Chronic Cerebral Hypoperfusion: Mechanisms and Therapeutic Advances.CNS neuroscience & therapeutics · 2026Review
- A review of animal models of vascular dementia.Molecular biology reports · 2026Review
- From Adaptive Resilience to Catastrophic Systems Collapse: Endothelial Entropy, Ferroptotic Propagation, and the Maternal Point of No Return in Emergency Peripartum Hysterectomy.International journal of molecular sciences · 2026Review
- Experimental models of cerebral small vessel disease: Physiological constraints, translational challenges and future directions.The Journal of physiology · 2026Review
- Endogenous neuroprotection in vascular cognitive impairment and dementia.EBioMedicine · 2026Review
- Electroacupuncture Ameliorates Learning and Memory Deficits in Vascular Cognitive Impairment Rats Through Activation of the Supramammillary Nucleus-Dentate Gyrus Circuit.CNS neuroscience & therapeutics · 2026Article
- Acute Hypoxic Exposure May Contribute to Depressive-Like Behaviors in Mice Through Disruption of Gut Microbiota Homeostasis.Alpha psychiatry · 2026Article
- Heightened propofol sensitivity and distinct electroencephalographic signatures in patients with valvular heart disease.BMC anesthesiology · 2026Observational
- The 3D Genome Browser 2.0: an enhanced online platform for visualizing and analyzing 3D genome architecture.Nucleic acids research · 2026Article
- Chronic cerebral hypoperfusion induces venous dysfunction via EPAS1 regulation in mice.Nature communications · 2025Article
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Authors and funding
22 authors.
Funding
Abstract
Vascular dementia is the second most common form of dementia. Yet, the mechanisms by which cerebrovascular damage progresses are insufficiently understood. Here, we create bilateral common carotid artery stenosis in mice, which effectively impairs blood flow to the brain, a major cause of the disease. Through imaging and single-cell transcriptomics of the mouse cortex, we uncover that blood vessel venous cells undergo maladaptive structural changes associated with increased Epas1 expression and activation of developmental angiogenic pathways. In a human cell model comparing arterial and venous cells, we observe that low-oxygen condition leads to sustained EPAS1 signaling specifically in venous cells. EPAS1 inhibition reduces cerebrovascular abnormalities, microglial activation, and improves markers of cerebral perfusion in vivo. In human subjects, levels of damaged endothelial cells from venous vessels are correlated with white matter injury in the brain and poorer cognitive functions. Together, these findings indicate EPAS1 as a potential therapeutic target to restore cerebrovascular integrity and mitigate neuroinflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.