Heme oxygenase-1: a therapeutic amplification funnel Fritz H. Bach Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA Correspondence: 99 Brookline Ave., Boston, MA 02215, USA. E-mail: fritz_bach@hms.harvard.edu HEME OXYGENASE -1 (HO-1) has emerged as a major "protective" gene, i.e., a gene that when expressed restores homeostasis in many situations by its anti-inflammatory, anti-apoptotic, and anti-proliferative actions (1) . The suggested use of HO-1 as a therapeutic is based on these attributes. The effects of HO-1 expression are mediated by one or more of the products of HO-1 degradation of heme: carbon monoxide (CO), biliverdin, and free iron (Fe 2+ ) (<h3>Fig. 1</h3> ). Biliverdin is converted to bilirubin by biliverdin reductase and the Fe 2+ leads to the opening of channels that export Fe 2+ from the cell as well as up-regulation of ferritin, an iron binding protein. Each product has been shown to have at least some of the protective properties of HO-1 expression. CO, biliverdin, and bilirubin can be administered as such in vitro or in vivo. The action of ferritin is usually mimicked by use of an iron binding compound such as desferioxamine or apoferritin, although studies have been done using a
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Heme oxygenase-1: a therapeutic amplification funnel
Bach, Fritz H.
Follow The FASEB Journal
, Volume 19 (10): 1216
Fed of American Socs for Experimental Biology – Aug 1, 2005
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