Format

Send to

Choose Destination
See comment in PubMed Commons below
Prog Retin Eye Res. 2014 Sep;42:85-102. doi: 10.1016/j.preteyeres.2014.05.002. Epub 2014 Jun 4.

Emerging role of advanced glycation-end products (AGEs) in the pathobiology of eye diseases.

Author information

1
Department of Biological Chemistry, University of Athens Medical School, Athens, Greece.
2
Department of Ophthalmology, School of Medicine, Aristotle University of Thessaloniki, 'AHEPA' Hospital, Thessaloniki, Greece.
3
Department of Biological Chemistry, University of Athens Medical School, Athens, Greece. Electronic address: papavas@med.uoa.gr.

Abstract

Advanced glycation end products (AGEs) have been implicated in vision loss associated with macula degeneration, cataract formation, diabetic retinopathy and glaucoma. This pathogenic potential is mainly attributed to their accumulation in ocular tissues where they mediate aberrant crosslinking of extracellular matrix proteins and disruption of endothelial junctional complexes that affects cell permeability, mediates angiogenesis and breakdown of the inner blood-retinal barrier. Furthermore, AGEs severely affect cellular metabolism by disrupting ATP production, enhancing oxidative stress and modulating gene expression of anti-angiogenic and anti-inflammatory genes. Elucidation of AGE-induced mechanisms of action in different eye compartments will help in the understanding of the complex cellular and molecular processes associated with eye diseases. Several pharmaceutical agents with anti-glycating and anti-oxidant properties as well as AGE crosslink 'breakers' have been currently applied to eye diseases. The role of diet and the beneficial effects of certain nutriceuticals provide an alternative way to manage chronic visual disorders that affect the quality of life of millions of people.

KEYWORDS:

AGEs; Angiogenesis; Anti-glycating agents; Blood-retinal barrier; Eye disease; Inflammation

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center