ArticleCell death & disease2025
Astrocytic YAP prevents the glutamate neurotoxicity by upregulation of EAAT2 expression and promotes the gain of stemness in astrocytes in ischemic stroke mice.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Endothelial YAP Signaling Promotes Blood-Spinal Cord Barrier Repair in Mice After Spinal Cord Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Hippo-YAP/TAZ Signaling in Astrocytes and Microglia: Role in Neuroinflammation, Neurodegeneration and Glial Tumors.International journal of molecular sciences · 2026Review
- YAP1 in control: how RNA networks and protein modifications shape its function and therapeutic targetability.Molecular cancer · 2026Review
- Sodium oligomannate reduces cerebral infarction and improves neurological function through microbiota remodeling in MCAO/R rats.Frontiers in pharmacology · 2026Article
- The Endocannabinoid-Microbiota-Neuroimmune Super-System: A Unifying Feedback Architecture for Systems Resilience, Collapse Trajectories, and Precision Feedback Medicine.International journal of molecular sciences · 2025Review
- Electroacupuncture Alleviates Cerebral Ischemia-Reperfusion Injury by Downregulating IL-17 A and Inhibiting Neurotoxic Astrocyte Activation.Neurochemical research · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
The excessive glutamate-mediated excitotoxicity is a major cause of the neuron death in ischemic stroke (IS). Astrocytic glutamate transporter protein-1 (GLT-1, also named excitatory amino acid transporter 2, EAAT2) is essential for maintaining low extracellular glutamate and preventing glutamate neurotoxicity, while its expression is regulated by Yes-associated protein (YAP) signaling reported by our previous study. Recent studies have shown that ischemic injury of the brain induces the gain of stemness in astrocytes dependent on the de novo DNA methyltransferase DNMT3A, and YAP signaling contributes to DNA methylation remodeling upon mouse embryonic stem cell differentiation. However, it remains unknown the roles of astrocytic YAP signaling in IS and whether it regulates the glutamate-mediated excitotoxicity and the gain of stemness in astrocytes induced by IS. In this study, we found that IS was aggravated in YAP
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