Treating iron overload

New England Journal of Medicine

Volumn 368, Issue 24, 2013, Pages 2325-2327

  Camaschella, Clara ^a  

^a VITA SALUTE SAN RAFFAELE UNIVERSITY   (Italy)

Author keywords

[No Author keywords available]

Indexed keywords

HEMOGLOBIN ALPHA CHAIN; HEMOGLOBIN BETA CHAIN; HEPCIDIN;

ARTICLE; BETA THALASSEMIA; CELL MATURATION; CELL SURVIVAL; DOWN REGULATION; ERYTHROCYTE; ERYTHROID CELL; GENE; GENE EXPRESSION; GENE MUTATION; GENE TARGETING; HEMOCHROMATOSIS; HEMOGLOBIN BLOOD LEVEL; HUMAN; IRON CHELATION; IRON OVERLOAD; NONHUMAN; PHLEBOTOMY; PRIORITY JOURNAL; PROTEIN BLOOD LEVEL; TMPRSS6 GENE; TREATMENT INDICATION;

EID: 84878829062     PISSN: 00284793     EISSN: 15334406     Source Type: Journal    
DOI: 10.1056/NEJMcibr1304338     Document Type: Article

References (5)

1. Schmidt PJ, Toudjarska I, Sendamarai AK, et al. An RNAi therapeutic targeting Tmprss6 decreases iron overload in Hfe (-/-) mice and ameliorates anemia and iron overload in murine β-thalassemia intermedia. Blood 2013;121:1200-8.
2. Guo S, Casu C, Gardenghi S, et al. Reducing TMPRSS6 ameliorates hemochromatosis and β-thalassemia in mice. J Clin Invest 2013;123:1531-41.
3. Ramos E, Ruchala P, Goodnough JB, et al. Minihepcidins prevent iron overload in a hepcidin-deficient mouse model of severe hemochromatosis. Blood 2012;120:3829-36.
4. Finberg KE, Whittlesey RL, Andrews NC. Tmprss6 is a genetic modifier of the Hfe-hemochromatosis phenotype in mice. Blood 2011;117:4590-9.
5. Nai A, Pagani A, Mandelli G, et al. Deletion of TMPRSS6 attenuates the phenotype in a mouse model of β-thalassemia. Blood 2012;119:5021-9.