Journal
AMINO ACIDS
Volume 42, Issue 4, Pages 1205-1220Publisher
SPRINGER WIEN
DOI: 10.1007/s00726-010-0778-x
Keywords
Lens; Retina; Aging; Diabetes; Cataract; Diabetic retinopathy; Age-related macular degeneration
Categories
Funding
- National Institutes of Health
- Ohio Lions Eye Research Foundation
- Action Medical Research
- Juvenile Diabetes Research Foundation (New York)
- Fight for Sight (UK)
- Medical Research Council
- Research to Prevent Blindness, New York
- Fight for Sight [1871/72] Funding Source: researchfish
- Medical Research Council [G0600053] Funding Source: researchfish
- MRC [G0600053] Funding Source: UKRI
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The proteins of the human eye are highly susceptible to the formation of advanced glycation end products (AGEs) from the reaction of sugars and carbonyl compounds. AGEs progressively accumulate in the aging lens and retina and accumulate at a higher rate in diseases that adversely affect vision such as, cataract, diabetic retinopathy and age-related macular degeneration. In the lens AGEs induce irreversible changes in structural proteins, which lead to lens protein aggregation and formation of high-molecular-weight aggregates that scatter light and impede vision. In the retina AGEs modify intra- and extracellular proteins that lead to an increase in oxidative stress and formation of pro-inflammatory cytokines, which promote vascular dysfunction. This review outlines recent advances in AGE research focusing on the mechanisms of their formation and their role in cataract and pathologies of the retina. The therapeutic action and pharmacological strategies of anti-AGE agents that can inhibit or prevent AGE formation in the eye are also discussed.
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