ArticleMolecular neurobiology2023
Rnf-213 Knockout Induces Pericyte Reduction and Blood-Brain Barrier Impairment in Mouse.
Article in Molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Mitophagy alleviates neuronal damage after subarachnoid hemorrhage: Role of autophagy-targeting chimera 4.Neural regeneration research · 2026Article
- An Rnf213-deficient hypoperfusion model reveals Moyamoya-relevant neurovascular remodeling.Angiogenesis · 2026Article
- Article
- HGSNAT alleviates oxygen-glucose deprivation- induced endothelial injury by suppressing ER stress: implications for Moyamoya disease.Frontiers in molecular neuroscience · 2026Article
- Moyamoya Disease and the Risk of Parkinson's Disease.Annals of clinical and translational neurology · 2025Article
- Moyamoya disease: epidemiology, clinical features, pathogenesis, diagnosis and therapeutic interventions.Molecular biomedicine · 2025Review
- RNF213 regulates blood‒brain barrier integrity by targeting TRAF3 for type I interferon activation during A. baumannii infection.PLoS pathogens · 2025Article
- The role of the RING finger protein 213 gene in Moyamoya disease.Fluids and barriers of the CNS · 2025Review
- ExploringBiomedicines · 2024Review
- HAPLN3 p.T34A contributes to incomplete penetrance of moyamoya disease in Chinese carrying RNF213 p.R4810K.European journal of neurology · 2024Article
- Blood-brain barrier disruption: a culprit of cognitive decline?Fluids and barriers of the CNS · 2024Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Moyamoya disease (MMD) is a rare cerebrovascular disorder characterized by progressive occlusion of the internal carotid artery and the formation of an abnormal compensatory capillary network at the base of the brain. Genomics studies identified Ring finger protein 213 (RNF213) as a common genetic factor that increases the susceptibility to MMD in East Asian people. However, the function of RNF213 and its roles in pathogenesis of MMD is unclear. Here, we showed that genetic knockout of Rnf213 in mice causes significant pericyte reduction and blood-brain barrier impairment in the cortex. These phenotypes are accompanied with microglia activation and elevated level of proinflammatory cytokines. Additionally, Rnf213-deficient mice showed reduced expression of tight junction proteins, including Occludin, Claudin-5, and ZO-1. Together, these data suggested that RNF213 might contribute to the pathogenesis of MMD through disruption of pericyte homeostasis and blood-brain barrier integrity by dysregulation of inflammatory responses and tight junction formation.
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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.