Heme oxygenase-1/CO as protective mediators in cigarette smoke- induced lung cell injury and chronic obstructive pulmonary disease

Tamás Dolinay, Augustine M K Choi , Stefan W. Ryter

Research output: Contribution to journalArticlepeer-review

32 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)769-776
Number of pages8
JournalCurrent Pharmaceutical Biotechnology
Volume13
Issue number6
DOIs
StatePublished - Jan 1 2012

Keywords

  • Apoptosis
  • Carbon monoxide
  • Chronic obstructive pulmonary disease
  • Cigarette smoke
  • Heme oxygenase-1
  • Lung
  • Reactive oxygen species

ASJC Scopus subject areas

  • Biotechnology
  • Pharmaceutical Science

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