The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Mitochondrial Dysfunction and Glaucoma
Abstract
Glaucoma is increasingly recognized as a neurodegenerative disorder, characterized by the accelerated loss of retinal ganglion cells (RGCs) and their axons. Open angle glaucoma prevalence and incidence increase exponentially with increasing age, yet the pathophysiology underlying increasing age as a risk factor for glaucoma is not well understood. Accumulating evidence points to age-related mitochondrial dysfunction playing a key role in the etiology of other neurodegenerative disorders including amyotrophic lateral sclerosis, Alzheimer and Parkinson disease. The 2 major functions of mitochondria are the generation of ATP through oxidative phosphorylation and the regulation of cell death by apoptosis. This review details evidence to support our hypothesis that age-associated mitochondrial dysfunction renders RGCs susceptible to glaucomatous injury by reducing the energy available for repair processes and predisposing RGCs to apoptosis. Eliciting the role of mitochondria in glaucoma pathogenesis may uncover novel therapeutic targets for protecting the optic nerve and preventing vision loss in glaucoma.
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Cites
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Energy metabolism of the visual system
Wong-Riley, M. (2010) · Eye and Brain · doi:10.2147/eb.s9078 · Cited by 461
Resveratrol: A miraculous natural compound for diseases treatment
Koushki, M., Amiri‐Dashatan, N., Ahmadi, N., Abbaszadeh, H., & Rezaei‐Tavirani, M. (2018) · Food Science & Nutrition · doi:10.1002/fsn3.855 · Cited by 316
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Metadata
- Authors
- Kong, G. Y. X., Van Bergen, N. J., Trounce, I. A., & Crowston, J. G.
- Venue
- Journal of Glaucoma
- Published
- 2009-02
- Volume
- 18
- Issue
- 2
- Pages
- 93-100
- ISSN
- 1057-0829 (ISSN-L)
- OpenAlex
- W1966110033
- Cited by
- 261
- References
- 12
- FWCI
- 18.37
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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