Journal
BLOOD
Volume 124, Issue 4, Pages 479-482Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2014-05-516252
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Funding
- National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases [R01 DK90554]
- American Society of Hematology (ASH)
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Although most circulating iron in blood plasma is destined for erythropoiesis, the mechanisms by which erythropoietic demand modulates the iron supply (erythroid regulators) remain largely unknown. Iron absorption, plasma iron concentrations, and tissue iron distribution are tightly controlled by the liver-produced hormone hepcidin. During the last decade, much progress has been made in elucidating hepcidin regulation by iron and inflammation. This review discusses the less understood mechanisms and mediators of hepcidin suppression in physiologically and pathologically stimulated erythropoiesis.
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