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. 2023 Apr 7;47(7):554–563. doi: 10.1038/s41366-023-01299-0

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Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Hepcidin, produced primarily by hepatocytes, reduces iron efflux from cells and duodenal iron absorption by reducing the stability of the ferroportin transporter (green). Hepcidin is mainly regulated via the bone morphogenic protein (BMP)/SMAD signalling pathway. The inflammatory cytokine interleukin-6 (IL-6) induces hepcidin. In response to cellular hypoxia the kidneys release erythropoietin (EPO), which stimulates erythropoiesis and the production of erythroferrone from erythroblasts. Erythroferrone inhibits hepcidin release, thereby increasing iron absorption and release of iron from stores. Image created in Biorender.com.