The continuous turnover of erythrocyte iron requires intercommunication between multiple cell types for homeostasis, including cells participating in iron uptake (enterocytes), utilization (erythroid precursors), recycling (reticuloendothelial macrophages), and storage (hepatocytes).… Click to show full abstract
The continuous turnover of erythrocyte iron requires intercommunication between multiple cell types for homeostasis, including cells participating in iron uptake (enterocytes), utilization (erythroid precursors), recycling (reticuloendothelial macrophages), and storage (hepatocytes). Coordination of iron flux between these cell types is determined by the regulated expression of the hepatocellular hormone hepcidin. In this issue of Blood, 2 research teams, Canali et al and Koch et al, independently demonstrate a key role in iron homeostasis by a cell type that might otherwise seem a bystander. Their studies provide convincing evidence that the source of bone morphogenetic proteins (BMPs) essential to basal and iron-regulated hepcidin expression is liver sinusoidal endothelial cells (LSECs).1,2
               
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