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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Heme oxygenase-1 and carbon monoxide in pulmonary medicine | Respiratory Research BioMed Central Review Open Access Heme oxygenase-l and carbon monoxide in pulmonary medicine Dirk-Jan Slebos1 Stefan W Ryter2 and Augustine MK Choi 2 Address Department of Pulmonary Diseases University Hospital Groningen Groningen The Netherlands and 2Pulmonary Allergy and Critical Care Medicine University of Pittsburgh School of Medicine Pittsburgh PA USA Email Dirk-Jan Slebos - choiam@msx.upmc.edu Stefan W Ryter - choiam@msx.upmc.edu Augustine MK Choi - choiam@msx.upmc.edu Corresponding author Published 07 August 2003 Received 27 May 2003 Accepted 07 August 2003 Respiratory Research 2003 4 7 This article is available from http respiratory-research.cOm content 4 1 7 2003 Slebos et al licensee BioMed Central Ltd. This is an Open Access article verbatim copying and redistribution of this article are permitted in all media for any purpose provided this notice is preserved along with the article s original URL. Abstract Heme oxygenase-1 HO-I an inducible stress protein confers cytoprotection against oxidative stress in vitro and in vivo. In addition to its physiological role in heme degradation HO-1 may influence a number of cellular processes including growth inflammation and apoptosis. By virtue of anti-inflammatory effects HO-1 limits tissue damage in response to proinflammatory stimuli and prevents allograft rejection after transplantation. The transcriptional upregulation of HO-1 responds to many agents such as hypoxia bacterial lipopolysaccharide and reactive oxygen nitrogen species. HO-1 and its constitutively expressed isozyme heme oxygenase-2 catalyze the rate-limiting step in the conversion of heme to its metabolites bilirubin IXa ferrous iron and carbon monoxide CO . The mechanisms by which HO-1 provides protection most likely involve its enzymatic reaction products. Remarkably administration of CO at low concentrations can substitute for HO-1 with respect to anti-inflammatory and anti-apoptotic effects suggesting a role for CO as a key
