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Published ahead of print on September 15, 2006, doi:10.1165/rcmb.2006-0333TR

Am. J. Respir. Cell Mol. Biol., Volume 36, Number 2, February 2007, 175-182

A more recent version of this article appeared on February 1, 2007
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Submitted on September 5, 2006
Revised on September 15, 2006

Carbon Monoxide and Bilirubin: Potential Therapies for Pulmonary/Vascular Injury and Disease

Stefan W Ryter1*, Danielle Morse1, and Augustine M.K. Choi1

1 Department of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA, USA

* To whom correspondence should be addressed. E-mail: ryters{at}upmc.edu.

Heme oxygenase-1 (HO-1), an inducible low-molecular-weight stress protein, confers cellular and tisssue protection in multiple models of injury and disease, including oxidative or inflammatory lung injury, ischemia/reperfusion injuries, and vascular injury/disease. The tissue protection provided by HO-1 potentially relates to the endogenous production of the end-products of its enzymatic activity: namely biliverdin/bilirubin, carbon monoxide (CO), and iron. Of these, CO and biliverdin/bilirubin show promise as possible therapeutic agents when applied exogenously in models of lung or vascular injury. CO activates intracellular signaling pathways involving soluble guanylate cyclase, and/or p38 mitogen activated protein kinase. While toxic at elevated concentration, low concentrations of CO can confer anti-inflammatory, antiapoptotic, anti-proliferative, and vasodilatory effects. Biliverdin and bilirubin are natural antioxidants that can provide protection against oxidative stress in cell culture and in plasma. Application of biliverdin or bilirubin protects against ischemia/reperfusion injury in several organ models. Recent evidence has also demonstrated anti-inflammatory and anti-proliferative properties of these pigments. To date, evidence has accumulated for salutary effects of CO, biliverdin and/or bilirubin in lung/vascular injury models, as well as in models of transplant-associated ischemia/reperfusion injury. Thus, the exogenous application of heme oxygenase end-products may provide an alternative to pharmacological or gene-therapy approaches to harness the therapeutic potential of HO-1.




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