Reciprocal regulation between hepcidin and erythropoiesis and its therapeutic application in erythroid disorders

Experimental Hematology
Caiyi WangHuiyong Chen

Abstract

Iron is required for hemoglobin production, and it plays a key role during erythropoiesis. Systemic iron homeostasis is mainly negatively regulated by the peptide hormone hepcidin, coded by the gene HAMP. Hepcidin excess may cause iron deficiency, iron-restricted erythropoiesis, and anemia. Conversely, hepcidin insufficiency leads to iron overload and oxidative damage in multiple tissues. During regulation of hepcidin synthesis, multiple promoter elements in the HAMP gene respond to variable signaling pathways corresponding to different extracellular situations. It has been reported that hepcidin expression can be suppressed by secreted erythroid factors, including GDF15, TWSG1, GDF11, and ERFE, thereby increasing iron availability for hemoglobin synthesis. These potential erythroid factors act via intricate mechanisms that remain controversial. However, it is clear that hepcidin affects erythropoiesis, and promising therapies targeting hepcidin have been developed to treat erythroid disorders. These therapeutic strategies include suppressing or activating HAMP gene expression, mimicking or activating hepcidin activity, and blocking the ability of hepcidin to bind to its target ferroportin.

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Citations

Mar 16, 2018·Current Opinion in Cardiology·Carles Díez-LópezJosé González-Costello
Sep 1, 2019·Medicinal Research Reviews·Zhong-Ming Qian, Ya Ke
Jan 17, 2019·Biological Trace Element Research·Wangqing ChenWu Zhu
Aug 28, 2021·International Journal of Molecular Sciences·Luc RochetteCatherine Vergely

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