Heat shock proteins, immunity and glaucoma
Abstract
Glaucoma is no longer viewed simply as elevated intraocular pressure (IOP) that damages the optic nerve. In addition to high IOP, evidence is rapidly accumulating that suggests damage to the optic nerve may be initiated or sustained by any number of factors including ischemia, excitotoxicity, neurotrophin insufficiency, peroxynitrite damage or others not yet defined. These different harmful influences then likely act through common final pathways that eventually activate the cellular proteases that accompany neuronal programmed cell death. We believe aberrant immune signal processing may also result in retinal ganglion cell death. We hypothesized that one form of glaucoma may be an autoimmune neuropathy in which an individual's immune system is not only inappropriately regulated, but a cytotoxic effect is rendered by the very system which normally serves to protect it against stress. We propose that the family of proteins termed "heat shock proteins" are critical modulators of both the homeostatic/cytoprotective as well as pathogenic/neurodegenerative arms of the immune system in retinal ganglion cells or glial cells and are thus integral to glaucomatous neurodegeneration.
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The serum of glaucoma patients contains high levels of antibodies, including against HSPs.
“The serum of glaucoma patients has been found to contain high levels of antibodies (e.g., against HSPs; Maruyama et al., 2000; Wax et al., 2001; Tezel et al., 2004; Grus et al., 2008).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Tezel et al., 2004
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The GG genotype of the HSPA1B gene is associated with increased risk of glaucoma in northern Iran
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Levels of Antibodies against Human Heat Shock Protein (HSP) 60 in Patients with Glaucoma in Poland
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Systemic Diseases and Glaucoma
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Systemic Diseases and Glaucoma
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The Link Between Gastrointestinal Microbiome And Ocular Disorders - A ReviewPreprint
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- Authors
- Tezel, G., Yang, J., & Wax, M. B.
- Affiliations
- University of Louisville (US)
- Washington University in St. Louis (US)
- Corresponding author
- Wax, Martin B.
- Venue
- Brain Research Bulletin
- Publisher
- Elsevier BV
- Published
- 2004-02
- Volume
- 62
- Issue
- 6
- Pages
- 473-480
- ISSN
- 0361-9230 (ISSN-L)
- OpenAlex
- W2031002260
- Cited by
- 66
- References
- 58
- Citations by year
- 2025: 1 · 2023: 3 · 2022: 3 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 3 · 2017: 4 · 2016: 5 · 2015: 4 · 2014: 4 · 2013: 5 · 2012: 2
- FWCI
- 1.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research Bulletin (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Eye Institute (EY012314, R01EY012314)
- Topics
- Health Sciences › Medicine › Ophthalmology › Glaucoma and retinal disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- heat shock proteins, glaucoma, retinal ganglion cell death, optic nerve degeneration, autoimmune neuropathy, neurodegeneration, immune regulation, glial cells, excitotoxicity, ischemia, peroxynitrite, neurotrophins, programmed cell death, intraocular pressure
- MeSH terms
- Animals, Glaucoma, Heat-Shock Proteins, Humans, Immunity
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