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Hepcidin assures the balance of circulating and stored iron levels for multiple physiological processes including oxygen transport and erythropoiesis, while limiting the toxicity of excess iron. The liver is the major site where regulatory signals from iron, erythropoietic drive and inflammation are integrated to control hepcidin production. Pathologically, hepcidin dysregulation by genetic inactivation, ineffective erythropoiesis, or inflammation leads to diseases of iron deficiency or overload such as iron\u2010refractory iron\u2010deficiency anaemia, anaemia of inflammation, iron\u2010loading anaemias and hereditary haemochromatosis. In the present review, we discuss recent insights into the molecular mechanisms governing hepcidin regulation, how these pathways are disrupted in iron disorders, and how this knowledge is being used to develop novel diagnostic and therapeutic strategies.<\/jats:p>","DOI":"10.1111\/bjh.17252","type":"journal-article","created":{"date-parts":[[2020,12,15]],"date-time":"2020-12-15T10:45:27Z","timestamp":1608029127000},"page":"882-893","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":70,"title":["Physiological and pathophysiological mechanisms of hepcidin regulation: clinical implications for iron disorders"],"prefix":"10.1111","volume":"193","author":[{"given":"Yang","family":"Xu","sequence":"first","affiliation":[{"name":"Division of Nephrology Program in Membrane Biology Massachusetts General Hospital Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"V\u00edctor 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