Cellular signaling and factors involved in Müller cell gliosis: neuroprotective and detrimental effects
Abstract
Müller cells are active players in normal retinal function and in virtually all forms of retinal injury and disease. Reactive Müller cells protect the tissue from further damage and preserve tissue function by the release of antioxidants and neurotrophic factors, and may contribute to retinal regeneration by the generation of neural progenitor/stem cells. However, Müller cell gliosis can also contribute to neurodegeneration and impedes regenerative processes in the retinal tissue by the formation of glial scars. This article provides an overview of the neuroprotective and detrimental effects of Müller cell gliosis, with accounts on the cellular signal transduction mechanisms and factors which are implicated in Müller cell-mediated neuroprotection, immunomodulation, regulation of Müller cell proliferation, upregulation of intermediate filaments, glial scar formation, and the generation of neural progenitor/stem cells. A proper understanding of the signaling mechanisms implicated in gliotic alterations of Müller cells is essential for the development of efficient therapeutic strategies that increase the supportive/protective and decrease the destructive roles of gliosis.
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Mammalian Müller glia usually mount a reactive gliotic response to injury that often does more harm than good.
“MG of the mammalian retina exhibit a reactive gliotic response to injury that often causes more harm than good”
From HB-EGF is Necessary and Sufficient for Müller Glia Dedifferentiation and Retina Regeneration (2012) · cites this paper as Bringmann et al., 2009
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BackgroundInfluentialMüller Glia in Retinal Innate Immunity: A Perspective on Their Roles in Endophthalmitis
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TNFα activates MAPK and Jak-Stat pathways to promote mouse Müller cell proliferation.
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Vision-related convergent gene losses reveal SERPINE3’s unknown role in the eye
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ERK1/2 pathway is activated in degenerated Rpe65-deficient mice
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- Authors
- Bringmann, A., Iandiev, I., Pannicke, T., Wurm, A., Hollborn, M., Wiedemann, P., Osborne, N. N., & Reichenbach, A.
- Affiliations
- University Hospital Leipzig (DE)
- Leipzig University (DE)
- University of Oxford (GB)
- Corresponding author
- Bringmann, Andreas
- Venue
- Progress in Retinal and Eye Research
- Publisher
- Elsevier BV
- Published
- 2009-11
- Volume
- 28
- Issue
- 6
- Pages
- 423-451
- ISSN
- 1350-9462 (ISSN-L)
- OpenAlex
- W2080816502
- Cited by
- 761
- References
- 543
- Citations by year
- 2026: 46 · 2025: 55 · 2024: 66 · 2023: 53 · 2022: 53 · 2021: 64 · 2020: 61 · 2019: 44 · 2018: 42 · 2017: 40 · 2016: 39 · 2015: 37 · 2014: 37 · 2013: 40 · 2012: 33
- FWCI
- 2.06
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Progress in Retinal and Eye Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Health Sciences › Medicine › Ophthalmology › Glaucoma and retinal disorders
- Keywords
- Müller cells, gliosis, retinal damage, neuroprotection, glial scar formation, retinal regeneration, neural progenitor cells, retinal stem cells, signal transduction, intermediate filaments, immunomodulation, neurodegeneration
- MeSH terms
- Animals, Gliosis, Humans, Neuroglia, Retinal Diseases, Signal Transduction, Up-Regulation, Neuroprotective Agents
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