Inhibition of heme oxygenase ameliorates anemia and reduces iron overload in a β-thalassemia mouse model

Author:

Garcia-Santos Daniel12ORCID,Hamdi Amel12ORCID,Saxova Zuzana3,Fillebeen Carine12,Pantopoulos Kostas12,Horvathova Monika3,Ponka Prem12ORCID

Affiliation:

1. Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, QC, Canada;

2. Department of Physiology, McGill University, Montreal, QC, Canada; and

3. Department of Biology, Faculty of Medicine and Dentistry, Palacky University, Olomouc, Czech Republic

Abstract

Key Points Iron released from heme by HO 1 contributes to the pathophysiology of thalassemia. Inhibition of HO 1 is of therapeutic value for the treatment of thalassemia.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Reference64 articles.

1. Non-transfusion-dependent thalassemias;Musallam;Haematologica,2013

2. A mouse model for beta 0-thalassemia;Yang;Proc Natl Acad Sci USA,1995

3. Ironing out ferroportin;Drakesmith;Cell Metab,2015

4. The heme oxygenase system: a regulator of second messenger gases;Maines;Annu Rev Pharmacol Toxicol,1997

5. The heme oxygenase system: update 2005;Maines;Antioxid Redox Signal,2005

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