Abstract
Cigarette smoking which exposes the lung to high concentrations of reactive oxidant species (ROS) is the major risk factor for chronic obstructive pulmonary disease (COPD). Recent studies indicate that the defense against oxidant stress is impaired in COPD and oxidant burden is increased in COPD even after smoking has ceased. ROS present in cigarette smoke interfere with protein folding in the endoplasmic reticulum thereby eliciting a compensatory response termed the “unfolded protein response.” The importance of the UPR lies in its ability to alter expression of a large number of gene programs involved in basic cellular processes including anti-oxidant defense. This article will review the several signaling pathways which mediate the unfolded protein response and, in particular, the role of the PERK (protein kinase R-like endoplasmic reticulum kinase) signaling pathway in protecting the lung against oxidant injury. Moreover, the impairment in oxidant defense present in the lung in COPD will be discussed.
Keywords: UPR, COPD, Smoke-Induced Oxidant Stress, Cigarette, reactive oxidant species, endoplasmic reticulum, DNA mutations, oxidant injury
Current Respiratory Medicine Reviews
Title: Cigarette Smoke-Induced Oxidant Stress in the Lung, the Unfolded Protein Response, and COPD
Volume: 7 Issue: 5
Author(s): Steven G. Kelsen and Salim Merali
Affiliation:
Keywords: UPR, COPD, Smoke-Induced Oxidant Stress, Cigarette, reactive oxidant species, endoplasmic reticulum, DNA mutations, oxidant injury
Abstract: Cigarette smoking which exposes the lung to high concentrations of reactive oxidant species (ROS) is the major risk factor for chronic obstructive pulmonary disease (COPD). Recent studies indicate that the defense against oxidant stress is impaired in COPD and oxidant burden is increased in COPD even after smoking has ceased. ROS present in cigarette smoke interfere with protein folding in the endoplasmic reticulum thereby eliciting a compensatory response termed the “unfolded protein response.” The importance of the UPR lies in its ability to alter expression of a large number of gene programs involved in basic cellular processes including anti-oxidant defense. This article will review the several signaling pathways which mediate the unfolded protein response and, in particular, the role of the PERK (protein kinase R-like endoplasmic reticulum kinase) signaling pathway in protecting the lung against oxidant injury. Moreover, the impairment in oxidant defense present in the lung in COPD will be discussed.
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Cite this article as:
G. Kelsen Steven and Merali Salim, Cigarette Smoke-Induced Oxidant Stress in the Lung, the Unfolded Protein Response, and COPD, Current Respiratory Medicine Reviews 2011; 7 (5) . https://dx.doi.org/10.2174/157339811797189786
DOI https://dx.doi.org/10.2174/157339811797189786 |
Print ISSN 1573-398X |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6387 |
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