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. 2014 Nov 29;14:187. doi: 10.1186/1471-2466-14-187

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© Stepaniants et al.; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Proposed model of dysregulation of the ubiquitin-proteasome system leading to the pathogenesis and progression of emphysema/COPD. Oxidative stress and inflammation induced by smoke, genetic or environmental insults result in dysregulation of ubiquitination-related genes and impairment of the proteasome function. Accumulation of abnormal proteins in the lung as a result of increased production and decreased degradation causes further damage of the proteasome function and dysregulation of UPS-related genes. Aberrant regulation of the UPS results in apoptosis, inflammation, and matrix remodeling, pathogenic characteristics of emphysema/COPD. Damaged proteasome function can also cause compensatory upregulation of genes associated with the UPS.