ArticleInternational journal of molecular sciences2021
VEGF-Independent Activation of Müller Cells by the Vitreous from Proliferative Diabetic Retinopathy Patients.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- FGF Signaling Potentiates Müller Glia for Mammalian Retinal Regeneration.bioRxiv : the preprint server for biology · 2026Article
- Molecular stress and neurovascular injury in the diabetic retina.The Journal of clinical investigation · 2026Review
- The pathogenesis of müller cell glial-mesenchymal transition in retinal fibrosis-related eye diseases.Frontiers in cell and developmental biology · 2026Review
- Mechanistic Insights into the Combined Anti-inflammatory Effects of Bevacizumab and Triamcinolone in Hyperglycemic Retinal Cells: Modulation of MCP-1, CXCL10, and Their Receptors.Journal of ophthalmic & vision research · 2026Article
- Multimodal imaging features of non-proliferative and proliferative diabetic retinopathy based on SD-OCT and fundus autofluorescence.Frontiers in medicine · 2026Article
- Targeting vascular endothelial growth receptor-2 (VEGFR-2): structural biology, functional insights, and therapeutic resistance.Archives of pharmacal research · 2025Review
- Differentiation of human hyalocytes from induced pluripotent stem cells through ascorbic acid treatment.Human cell · 2025Article
- Experimental and clinical tests of FDA-approved kinase inhibitors for the treatment of neurological disorders (update 2024).Exploration of drug science · 2025Article
- Aspirin-triggered DHA metabolites inhibit angiogenesis.Frontiers in pharmacology · 2025Article
- Retinal Inflammation and Reactive Müller Cells: Neurotrophins' Release and Neuroprotective Strategies.Biology · 2024Review
- Cell and molecular targeted therapies for diabetic retinopathy.Frontiers in endocrinology · 2024Review
- miR-26a-5p Attenuates Oxidative Stress and Inflammation in Diabetic Retinopathy through the USP14/NF-Journal of ophthalmology · 2024Article
- Effects of aflibercept and bevacizumab on cell viability, cell metabolism and inflammation in hypoxic human Müller cells.PloS one · 2024Article
- Müller cells and retinal angiogenesis: critical regulators in health and disease.Frontiers in cellular neuroscience · 2024Review
- Induced pluripotent stem cell-derived extracellular vesicles overexpressing SFPQ protect retinal Müller cells against hypoxia-induced injury.Cell biology and toxicology · 2023Article
- Elucidating glial responses to products of diabetes-associated systemic dyshomeostasis.Progress in retinal and eye research · 2023Review
- Diabetic Retinopathy: Soluble and Imaging Ocular Biomarkers.Journal of clinical medicine · 2023Review
- Pathophysiology and clinical aspects of epiretinal membrane - review.Frontiers in medicine · 2023Review
- FDA-Approved Kinase Inhibitors in Preclinical and Clinical Trials for Neurological Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Contribution of Müller Cells in the Diabetic Retinopathy Development: Focus on Oxidative Stress and Inflammation.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Proliferative diabetic retinopathy (PDR), a major complication of diabetes mellitus, results from an inflammation-sustained interplay among endothelial cells, neurons, and glia. Even though anti-vascular endothelial growth factor (VEGF) interventions represent the therapeutic option for PDR, they are only partially efficacious. In PDR, Müller cells undergo reactive gliosis, produce inflammatory cytokines/chemokines, and contribute to scar formation and retinal neovascularization. However, the impact of anti-VEGF interventions on Müller cell activation has not been fully elucidated. Here, we show that treatment of MIO-M1 Müller cells with vitreous obtained from PDR patients stimulates cell proliferation and motility, and activates various intracellular signaling pathways. This leads to cytokine/chemokine upregulation, a response that was not mimicked by treatment with recombinant VEGF nor inhibited by the anti-VEGF drug ranibizumab. In contrast, fibroblast growth factor-2 (FGF2) induced a significant overexpression of various cytokines/chemokines in MIO-M1 cells. In addition, the FGF receptor tyrosine kinase inhibitor BGJ398, the pan-FGF trap NSC12, the heparin-binding protein antagonist N-tert-butyloxycarbonyl-Phe-Leu-Phe-Leu-Phe Boc2, and the anti-inflammatory hydrocortisone all inhibited Müller cell activation mediated by PDR vitreous. These findings point to a role for various modulators beside VEGF in Müller cell activation and pave the way to the search for novel therapeutic strategies in PDR.
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