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Expert Review of Clinical Pharmacology Volume 5, 2012 - Issue 3
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Review

Strategies to decrease ongoing oxidant burden in chronic obstructive pulmonary disease

Irfan Rahman Department of Environmental Medicine, Lung Biology and Disease Program, University of Rochester Medical Center, Box 850, 601 Elmwood Avenue, Rochester, NY 14642, USA. [email protected]; Department of Environmental Medicine, Lung Biology and Disease Program, University of Rochester Medical Center, Box 850, 601 Elmwood Avenue, Rochester, NY 14642, USA. [email protected]
&
Vuokko L Kinnula Pulmonary Division, Department of Medicine, University of Helsinki and Helsinki University Central Hospital, Box 440, Stenbäckinkatu 9A, Helsinki 00029, Finland; Pulmonary Division, Department of Medicine, University of Helsinki and Helsinki University Central Hospital, Box 440, Stenbäckinkatu 9A, Helsinki 00029, Finland
Pages 293-309 | Published online: 10 Jan 2014
 
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Abstract

Chronic obstructive pulmonary disease (COPD) is a leading cause of mortality and morbidity globally, and its development is mainly associated with tobacco/biomass smoke-induced oxidative stress. Hence, targeting systemic and local oxidative stress with agents that can balance the antioxidant/redox system can be expected to be useful in the treatment of COPD. Preclinical and clinical trials have revealed that antioxidants/redox modulators can detoxify free radicals and oxidants, control expression of redox and glutathione biosynthesis genes, chromatin remodeling and inflammatory gene expression; and are especially useful in preventing COPD exacerbations. In this review, various novel approaches and problems associated with these approaches in COPD are reviewed.

Acknowledgements

The authors thank Jae-woong Hwang and Suzanne Bellanca for formatting the references.

Financial & competing interests disclosure

I Rahman is supported by the NIH 1R01HL085613, 1R01HL097751, 1R01HL09284 and NIEHS Environmental Health Science Center grant P30-ES01247. VL Kinnula is partly supported by a special governmental subsidy for health sciences research (HUCH-EVO) from Helsinki University Central Hospital and by the Finnish Antituberculosis Association Foundation. 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.

Notes

CDDO: 2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oic acid; CDDO-Im: 1[2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oyl]imidazole.

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