Journal
ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY
Volume 50, Issue -, Pages 323-354Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev.pharmtox.010909.105600
Keywords
free radicals; cell death; inflammation; immune-mediated inflammatory diseases
Categories
Funding
- Fundacao para a Ciencia e Tecnologia, Portugal [SFRH/BPD/44256/2008, POCTI/SAU-MNO/56066/2004, PTDC/SAU-MII/65765/2006]
- European Commission [PEOPLE-2007-2-1-IEF]
- European Community [LSH-2005-1.2.5-1]
- Germ Fund
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Heme oxygenases (140) catabolize free heme, that is, iron (Fe) protoporphyrin (IX), into equimolar amounts of Fe2+, carbon monoxide (CO), and biliverdin. The stress-responsive HO-1 isoenzyme affords protection against programmed cell death. The mechanism underlying this cytoprotective effect relies on the ability of HO-1 to catabolize free heme and prevent it from sensitizing cells to undergo programmed cell death. This cytoprotective effect inhibits the pathogenesis of a variety of immune-mediated inflammatory diseases.
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