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Review

Therapeutic Potential of Targeting Lipid Aldehydes and Lipoxidation End-Products in the Treatment of Ocular Disease

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Pages 189-211 | Published online: 30 Jan 2013
 

Abstract

Lipoxidation reactions and the subsequent accumulation of advanced lipoxidation end products (ALEs) have been implicated in the pathogenesis of many of the leading causes of visual impairment. Here, we begin by outlining some of the major lipid aldehydes produced through lipoxidation reactions, the ALEs formed upon their reaction with proteins, and the endogenous aldehyde metabolizing enzymes involved in protecting cells against lipoxidation mediated damage. Discussions are subsequently focused on the clinical and experimental evidence supporting the contribution of lipid aldehydes and ALEs in the development of ocular diseases. From these discussions, it is clear that inhibition of lipoxidation reactions and ALE formation could represent a new therapeutic avenue for the treatment of a broad range of ocular disorders. Current and emerging pharmacological strategies to prevent or neutralize the effects of lipid aldehydes and ALEs are therefore considered, with particular emphasis on the potential of these drugs for treatment of diseases of the eye.

Acknowledgements

The authors gratefully acknowledge P Har Yong and M Ward for their help with the immunolabelling and electroretinography studies, respectively.

Financial & competing interests disclosure

Work from the authors’ laboratories discussed in this article was supported by The Juvenile Diabetes Research Foundation (USA), Fight for Sight (UK) and The Northern Ireland Research and Development Office. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Ethical disclosure

All procedures with animals from the authors’ laboratories were approved by The Queen’s University of Belfast Animal Ethics Committee and were performed in accordance with the UK Animals (Scientific Procedures) Act, 1986.

Additional information

Funding

Work from the authors’ laboratories discussed in this article was supported by The Juvenile Diabetes Research Foundation (USA), Fight for Sight (UK) and The Northern Ireland Research and Development Office. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

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