ArticleThe European journal of neuroscience2009
Inactivation of astroglial NF-kappa B promotes survival of retinal neurons following ischemic injury.
Article in The European journal of neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed, 143 citations in OpenAlex.
- Dual role of microglia in glaucoma: Regulation of neuroinflammation and neuroregeneration.Neural regeneration research · 2026Article
- Identification of post-translational modification-related biomarkers in ischemic stroke using bioinformatics and machine learning.Scientific reports · 2025Article
- Targeting Connexin 43 in Retinal Astrocytes Promotes Neuronal Survival in Glaucomatous Injury.Glia · 2025Article
- Multilayered Nanocarriers as a New Strategy for Delivering Drugs with Protective and Anti-inflammatory Potential: Studies in Hippocampal Organotypic Cultures Subjected to Experimental Ischemia.Molecular neurobiology · 2025Article
- The impact of astrocytic NF-κB on healthy and Alzheimer's disease brains.Scientific reports · 2024Article
- Polar lipids modify Alzheimer's Disease pathology by reducing astrocyte pro-inflammatory signaling through platelet-activating factor receptor (PTAFR) modulation.Lipids in health and disease · 2024Article
- Astrocyte KDM4A mediates chemokines and drives neutrophil infiltration to aggravate cerebral ischemia and reperfusion injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Astrocyte Regulation of Neuronal Function and Survival in Stroke Pathophysiology.Advances in neurobiology · 2024Review
- Helicobacter pylori outer membrane vesicles induce astrocyte reactivity through nuclear factor-κappa B activation and cause neuronal damage in vivo in a murine model.Journal of neuroinflammation · 2023Article
- Multiple types of programmed necrosis such as necroptosis, pyroptosis, oxytosis/ferroptosis, and parthanatos contribute simultaneously to retinal damage after ischemia-reperfusion.Scientific reports · 2022Article
- Article
- The role of TIGAR in nervous system diseases.Frontiers in aging neuroscience · 2022Review
- Gap Junctional Coupling Between Retinal Astrocytes Exacerbates Neuronal Damage in Ischemia-Reperfusion Injury.Investigative ophthalmology & visual science · 2021Article
- Profiles of microRNA in aqueous humor of normal tension glaucoma patients using RNA sequencing.Scientific reports · 2021Article
- Beyond the GFAP-Astrocyte Protein Markers in the Brain.Biomolecules · 2021Review
- Review
- Neuroinflammation in Post-Ischemic Neurodegeneration of the Brain: Friend, Foe, or Both?International journal of molecular sciences · 2021Review
- Astrocyte Activation in Neurovascular Damage and Repair Following Ischaemic Stroke.International journal of molecular sciences · 2021Review
- Therapeutic Drugs and Devices for Tackling Ocular Hypertension and Glaucoma, and Need for Neuroprotection and Cytoprotective Therapies.Frontiers in pharmacology · 2021Review
- Neuroinflammation and Scarring After Spinal Cord Injury: Therapeutic Roles of MSCs on Inflammation and Glial Scar.Frontiers in immunology · 2021Review
32 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
Reactive astrocytes have been implicated in neuronal loss following ischemic stroke. However, the molecular mechanisms associated with this process are yet to be fully elucidated. In this work, we tested the hypothesis that astroglial NF-kappaB, a key regulator of inflammatory responses, is a contributor to neuronal death following ischemic injury. We compared neuronal survival in the ganglion cell layer (GCL) after retinal ischemia-reperfusion in wild-type (WT) and in GFAP-IkappaBalpha-dn transgenic mice, where the NF-kappaB classical pathway is suppressed specifically in astrocytes. The GFAP-IkappaBalpha-dn mice showed significantly increased survival of neurons in the GCL following ischemic injury as compared with WT littermates. Neuroprotection was associated with significantly reduced expression of pro-inflammatory genes, encoding Tnf-alpha, Ccl2 (Mcp1), Cxcl10 (IP10), Icam1, Vcam1, several subunits of NADPH oxidase and NO-synthase in the retinas of GFAP-IkappaBalpha-dn mice. These data suggest that certain NF-kappaB-regulated pro-inflammatory and redox-active pathways are central to glial neurotoxicity induced by ischemic injury. The inhibition of these pathways in astrocytes may represent a feasible neuroprotective strategy for retinal ischemia and stroke.
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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.