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. 2019 Oct 9;10:1294. doi: 10.3389/fphys.2019.01294

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Copyright © 2019 Pagani, Nai, Silvestri and Camaschella.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic representation of mechanisms of anemias with high (left panel) and low hepcidin (right panel). Panel (A). Molecular pathogenesis of anemia associated with high hepcidin levels. LSEC, liver sinusoidal endothelial cells producing bone morphogenetic proteins (BMPs); BMPRs, BMP receptors; IL6, interleukin 6; HC, hepatocytes; HAMP, hepcidin gene. Fe, iron; FPN, ferroportin; 1, IRIDA; 2, Anemia of inflammation; 3, hepcidin producing adenoma. Panel (B). Molecular pathogenesis of hepcidin variation in anemias due to ineffective erythropoiesis. ERFE, erythroferrone sequestering BMPs. Other mechanisms inhibiting hepcidin in this type of anemia, as decrease of transferrin saturation and hypoxia, are not shown. See text for details.

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