Oxidative damage and protection of the RPE.
By J. Cai, K. C. Nelson, Mei Wu, P. Sternberg, Dean P. Jones. Progress in retinal and eye research, 2000
655 citations recorded by the source corpus.
Subfields: Biochemistry, Clinical Biochemistry, Ophthalmology
View Paper: https://www.semanticscholar.org/paper/780e80dfb488a2a0c08ef4420c6cfcf46e52afec
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In Biochemistry
In Clinical Biochemistry
In Ophthalmology
Citations in the corpus
- The Impact of Oxidative Stress and Inflammation on RPE Degeneration in Non-neovascular AMD (2017, background): “Since RPE cells are predominantly post-mitotic, damaged mitochondria are not removed during cell division (Cai et al., 2000).”
- Para-inflammation in the aging retina. (2009, background): “ROS impair cell function by readily reacting with nucleic acids, lipids and proteins and may induce cell death in retinal ganglion cells, photoreceptor cells and RPE cells in pathological conditions (Cai et al., 2000; Krishnamoorthy et al., 1999; Li and Osborne, 2008; Sanvicens et al., 2004).”
- The Cystine/Glutamate Antiporter System xc − in Health and Disease: From Molecular Mechanisms to Novel Therapeutic Opportunities (2013, positive): “Oxidative stress to the RPE is implicated in the devastating disease age-related macular degeneration (AMD), and GSH protects these cells from oxidant-induced apoptosis [reviewed in (31)].”
- Current concepts in the pathogenesis of age-related macular degeneration. (2004, background): “Major antioxidants in the retina and RPE include water-soluble metabolites and enzymes (vitamin C [ascorbic acid], glutathione, catalase, glutathione peroxidase, and superoxide dismutase), lipidsoluble substances (vitamin E [ -tocopherol], retinoids [vitamin A derivatives], and carotenoids), and mel”