ArticleASN neuro
Disruption of Fractalkine Signaling Leads to Microglial Activation and Neuronal Damage in the Diabetic Retina.
Article in ASN neuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Effects of diabetes on microglial physiology: a systematic review of in vitro, preclinical and clinical studies.Journal of neuroinflammation · 2023Pooled it
- Vitreoretinal Myeloid Cell Heterogeneity: Diverse Roles in Homeostasis, Immune Surveillance, and Pathophysiology.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Relationship Between the Degree of Diabetic Retinopathy and Serum Fractalkine (CX3CL1) in Patients with Type 2 Diabetes: A Single-Center Cross-Sectional Study.Medicina (Kaunas, Lithuania) · 2026Article
- Neutrophil percentage to albumin ratio and advanced cardiovascular-kidney-metabolic syndrome in diabetes: a machine learning approach.European journal of medical research · 2025Article
- Crosstalk Between Neuronal and Glial Cells in Diabetic Retinopathy: Mechanisms and Implications for Neurodegeneration.Molecular neurobiology · 2025Review
- Special Issue "Fractalkine (CX3CL1) and Its Chemoattractant and Adhesion Molecule Properties in Health and Disease".International journal of molecular sciences · 2025Article
- Early-stage diabetic retinopathy: gut-metabolic triggers, immune-neurodegeneration, and interventions.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2025Review
- Genetic polymorphisms in human CXJournal of neuroinflammation · 2025Article
- Targeting glial fibrillary acidic protein in glaucoma: a monoclonal antibody approach to modulate glial reactivity and neuroinflammation for neuroprotection.Journal of neuroinflammation · 2025Article
- AAV-mediated inner ear gene delivery triggers mild host immune responses in the mammalian inner ear.Molecular therapy. Methods & clinical development · 2025Article
- CX3CR1-Fractalkine Dysregulation Affects Retinal GFAP Expression, Inflammatory Gene Induction, and LPS Response in a Mouse Model of Hypoxic Retinopathy.International journal of molecular sciences · 2025Article
- The Role of Fractalkine in Diabetic Retinopathy: Pathophysiology and Clinical Implications.International journal of molecular sciences · 2025Review
- Leukocyte recruitment in flavivirus-induced encephalitis.Frontiers in immunology · 2025Review
- Review
- The role of microglia in the development of diabetic retinopathy.npj metabolic health and disease · 2024Review
- Astrogliosis in the GFAP-CreBiomolecules · 2024Article
- Role of myeloid cells in ischemic retinopathies: recent advances and unanswered questions.Journal of neuroinflammation · 2024Review
- Fractalkine isoforms differentially regulate microglia-mediated inflammation and enhance visual function in the diabetic retina.Journal of neuroinflammation · 2024Article
- Therapeutic Delivery of Soluble Fractalkine Ameliorates Vascular Dysfunction in the Diabetic Retina.International journal of molecular sciences · 2024Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Fractalkine (CX3CL1 or FKN) is a membrane-bound chemokine expressed on neuronal membranes and is proteolytically cleaved to shed a soluble chemoattractant domain. FKN signals via its unique receptor CX3CR1 expressed on microglia and other peripheral leukocytes. The aim of this study is to determine the role of CX3CR1 in inflammatory-mediated damage to retinal neurons using a model of diabetic retinopathy. For this, we compared neuronal, microglial, and astroglial densities and inflammatory response in nondiabetic and diabetic (Ins2(Akita)) CX3CR1-wild-type and CX3CR1-deficient mice at 10 and 20 weeks of age. Our results show that Ins2(Akita) CX3CR1-knockout mice exhibited (a) decreased neuronal cell counts in the retinal ganglion cell layer, (b) increased microglial cell numbers, and (c) decreased astrocyte responses comparable with Ins2(Akita) CX3CR1-Wild-type mice at 20 weeks of age. Analyses of the inflammatory response using PCR arrays showed several inflammatory genes differentially regulated in diabetic tissues. From those, the response in Ins2(Akita) CX3CR1-deficient mice at 10 weeks of age revealed a significant upregulation of IL-1β at the transcript level that was confirmed by enzyme-linked immunosorbent assay in soluble retinal extracts. Overall, IL-1β, VEGF, and nitrite levels as a read out of nitric oxide production were abundant in Ins2(Akita) CX3CR1-deficient retina. Notably, double immunofluorescence staining shows that astrocytes act as a source of IL-1β in the Ins2(Akita) retina, and CX3CR1-deficient microglia potentiate the inflammatory response via IL-1β release. Collectively, these data demonstrate that dysregulated microglial responses in absence of CX3CR1 contribute to inflammatory-mediated damage of neurons in the diabetic retina.
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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.