Erythroferrone structure, function, and physiology: Iron homeostasis and beyond. Issue 7 (28th December 2020)

• Record Type: Journal Article
• Authors: Srole, Daniel N; Ganz, Tomas
• Is Part Of: Journal of cellular physiology. Volume 236:Issue 7(2021)
• Page Start: 4888
• Page End: 4901
• Publication Date: 2020-12-28
• Subjects: bone morphogenetic proteins -- erythroferrone -- hepcidin -- ineffective erythropoiesis -- iron homeostasis -- β‐thalassemia; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.30247
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract: Erythroferrone (ERFE) is the main erythroid regulator of hepcidin, the homeostatic hormone controlling plasma iron levels and total body iron. When the release of erythropoietin from the kidney stimulates the production of new red blood cells, it also increases the synthesis of ERFE in bone marrow erythroblasts. Increased ERFE then suppresses hepcidin synthesis, thereby mobilizing cellular iron stores for use in heme and hemoglobin synthesis. Recent mechanistic studies have shown that ERFE suppresses hepcidin transcription by inhibiting bone morphogenetic protein signaling in hepatocytes. In ineffective erythropoiesis, pathological overproduction of ERFE by an expanded population of erythroblasts suppresses hepcidin and causes iron overload, even in non‐transfused patients. ERFE may be a useful biomarker of ineffective erythropoiesis and an attractive target for treating its systemic effects. Abstract : Erythroferrone (ERFE) is the main erythroid regulator of hepcidin, the homeostatic hormone controlling plasma iron levels and total body iron. Recent mechanistic studies have shown that ERFE suppresses hepcidin transcription by inhibiting bone morphogenetic protein signaling in hepatocytes. ERFE may be a useful biomarker of ineffective erythropoiesis and an attractive target for treating its systemic effects.