{"id":101,"date":"2020-10-28T12:43:31","date_gmt":"2020-10-28T12:43:31","guid":{"rendered":"https:\/\/www.embl.org\/about\/info\/mmpu\/?page_id=101"},"modified":"2026-02-17T11:42:58","modified_gmt":"2026-02-17T11:42:58","slug":"iron-homeostasis","status":"publish","type":"page","link":"https:\/\/www.embl.org\/about\/info\/mmpu\/research-groups\/iron-homeostasis\/","title":{"rendered":"Iron Homeostasis"},"content":{"rendered":"\n
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Group leaders: Matthias W. Hentze and Martina Muckenthaler<\/h2>\n\n\n\n

Our research interest<\/h3>\n\n\n\n

As an essential nutrient and a potential toxin, iron poses an exquisite regulatory problem in biology and medicine. Disturbances of the delicate balancing systems for systemic and\/or local iron homeostasis are emerging as underlying causes of common hematological, metabolic and neurodegenerative diseases.<\/p>\n\n\n\n

Our research aims to understand the physiological control of cellular and systemic iron metabolism and its disturbances in human disease<\/p>\n\n\n\n

Background<\/h3>\n\n\n\n

Iron is essential for fundamental metabolic processes in cells and organisms. Regulation of systemic iron homeostasis evolved to maintain a plasma iron concentration that secures adequate supplies while preventing organ iron overload.<\/p>\n\n\n\n

The homeostatic system must react to signals from pathways that consume iron (e.g. the erythropoiesis) and send signals to cells that supply iron (e.g. duodenal enterocytes, which absorb iron from the diet; macrophages which recycle iron from senescent erythrocytes, and hepatocytes which are the major iron stores). The small hepatic peptide hormone hepcidin (Hamp, LEAP1) orchestrates these iron fluxes and controls the amount of available extracellular iron by interacting with the iron exporter ferroportin: binding of hepcidin induces ferroportin internalization and degradation, thus reducing the levels of iron in circulation.<\/p>\n\n\n\n

Goals<\/h3>\n\n\n\n

Our work is based on modern \u201comics\u201d analyses of cultured cells, animal models (mostly mouse) and clinical samples. Hypotheses generated in this way are then pursued for a more detailed understanding of regulatory mechanisms involved in iron homeostasis and the identification of novel regulators of iron metabolism. We then aim to translate new results into understanding human disease and to contribute to clinical patient management.<\/p>\n\n\n\n

Specifically, our current and future work will focus on four themes:<\/p>\n\n\n\n