ReviewAging and disease2024
Crosstalk Between Microglia and Müller Glia in the Age-Related Macular Degeneration: Role and Therapeutic Value of Neuroinflammation.
Review in Aging and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed.
- Myeloid deficiency of RORα exacerbates lipid dysregulation and laser-induced choroidal neovascularization.Angiogenesis · 2026Article
- Lysosomal channel TPC2 modulates microglia-endothelial signaling in choroidal angiogenesis.Angiogenesis · 2026Article
- Redefining ocular safety assessment: retinal organoids as platforms for predicting human ocular toxicology.Genes & genomics · 2026Review
- Intriguing roles of Müller glia: a special emphasis on the development and pathology of Müller glia cells in the retina.International ophthalmology · 2026Review
- Age-Related Neurovascular Dysfunction in the Retina and Potential Pathogenic Mechanisms.Investigative ophthalmology & visual science · 2026Review
- Complement, Inflammasome, and Microglial Crosstalk in Glaucoma: From Neurodegeneration to Immune-Based Precision Therapy.Life (Basel, Switzerland) · 2026Review
- The role of NLRP3 inflammasome in age-related macular degeneration: mechanisms and therapeutic prospects.Frontiers in aging neuroscience · 2026Review
- Tumor Necrosis Factor Alpha-Mediated Interaction Between Microglia and Müller Cells Exacerbates Retinal Ganglion Cell Damage in Experimental Glaucoma.Neuroscience bulletin · 2026Article
- Crosstalk Between Neuronal and Glial Cells in Diabetic Retinopathy: Mechanisms and Implications for Neurodegeneration.Molecular neurobiology · 2025Review
- Intermittent fasting attenuates glial hyperactivation and photoreceptor degeneration in a NaIOCommunications biology · 2025Article
- ScReNI: Single-cell Regulatory Network Inference Through Integrating scRNA-seq and scATAC-seq Data.Genomics, proteomics & bioinformatics · 2025Article
- Integrative Multiomics Identifies CD64⁺ Monocytes as Potential Contributors to Age-Related Macular Degeneration.Investigative ophthalmology & visual science · 2025Article
- Co-delivery of antioxidants and siRNA-VEGF: promising treatment for age-related macular degeneration.Drug delivery and translational research · 2025Review
- Latent epigenetic programs in Müller glia contribute to stress and disease response in the retina.Developmental cell · 2025Article
- Anti-TNFα and Anti-IL-1β Monoclonal Antibodies Preserve BV-2 Microglial Homeostasis Under Hypoxia by Mitigating Inflammatory Reactivity and ATF4/MAPK-Mediated Apoptosis.Antioxidants (Basel, Switzerland) · 2025Article
- Review
- Retinal Inflammation and Reactive Müller Cells: Neurotrophins' Release and Neuroprotective Strategies.Biology · 2024Review
- Imaging the eye as a window to brain health: frontier approaches and future directions.Journal of neuroinflammation · 2024Review
- Advancing Neurological Health: Insights into Aging, Immunity, and Vascular Dynamics.Aging and disease · 2024Article
- Tyrosine Kinase Receptor ErbB4 in Advillin-Positive Neurons Contributes to Inflammatory Pain Hypersensitivity in Mouse DRG.Aging and disease · 2023Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-related macular degeneration (AMD) is a progressive neurodegeneration disease that causes photoreceptor demise and vision impairments. In AMD pathogenesis, the primary death of retinal neurons always leads to the activation of resident microglia. The migration of activated microglia to the ongoing retinal lesion and their morphological transformation from branching to ameboid-like are recognized as hallmarks of AMD pathogenesis. Activated microglia send signals to Müller cells and promote them to react correspondingly to damaging stimulus. Müller cells are a type of neuroglia cells that maintain the normal function of retinal neurons, modulating innate inflammatory responses, and stabilize retinal structure. Activated Müller cells can accelerate the progression of AMD by damaging neurons and blood vessels. Therefore, the crosstalk between microglia and Müller cells plays a homeostatic role in maintaining the retinal environment, and this interaction is complicatedly modulated. In particular, the mechanism of mutual regulation between the two glia populations is complex under pathological conditions. This paper reviews recent findings on the crosstalk between microglia and Müller glia during AMD pathology process, with special emphasis on its therapeutic potentials.
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Registered trials
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