Heme Oxygenase-1/CO as Protective Mediators in Cigarette Smoke- Induced Lung Cell Injury and Chronic Obstructive Pulmonary Disease

Title:Heme Oxygenase-1/CO as Protective Mediators in Cigarette Smoke- Induced Lung Cell Injury and Chronic Obstructive Pulmonary Disease

Volume: 13 Issue: 6

Author(s): Tamas Dolinay, Augustine M.K. Choi and Stefan W. Ryter

Affiliation:

Keywords: Apoptosis, carbon monoxide, chronic obstructive pulmonary disease, cigarette smoke, heme oxygenase-1, lung, reactive oxygen species

Abstract: Chronic obstructive pulmonary disease (COPD) is a disease involving airways restriction, alveolar destruction, and loss of lung function, primarily due to cigarette smoke (CS) exposure. The inducible stress protein heme oxygenase-1 (HO-1) has been implicated in cytoprotection against the toxic action of many xenobiotics, including CS. HO-1 also protects against elastase-induced emphysema. Differential expression of HO-1 in epithelial cells and macrophages may contribute to COPD susceptibility. Genetic polymorphisms in the HO-1 gene, which may account for variations in HO-1 expression among subpopulations, may be associated with COPD pathogenesis. Carbon monoxide (CO), a primary reaction product of HO-1 has been implicated in cytoprotection in many acute lung injury models, though it’s precise role in chronic CS-induced lung injury remains unclear. CO is a potential biomarker of CS exposure and of inflammatory lung conditions. To date, a single clinical trial has addressed the possible therapeutic potential of CO in COPD patients. The implications of the cytoprotective potential of HO-1/CO system in CS-induced lung injury and COPD are discussed.

Cite this article as:

Dolinay Tamas, M.K. Choi Augustine and W. Ryter Stefan, Heme Oxygenase-1/CO as Protective Mediators in Cigarette Smoke- Induced Lung Cell Injury and Chronic Obstructive Pulmonary Disease, Current Pharmaceutical Biotechnology 2012; 13 (6) . https://dx.doi.org/10.2174/138920112800399338