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, 112 (2), 219-30

Forging a Field: The Golden Age of Iron Biology


Forging a Field: The Golden Age of Iron Biology

Nancy C Andrews. Blood.


Figure 1
Figure 1
Overview of iron homeostasis. The central portion of the figure depicts the flow of iron into the body (through the small intestine), to transferrin (Tf), to the major site of utilization (the erythroid bone marrow), to circulating erythrocytes, to tissue macrophages that phagocytose senescent erythrocytes and recycle iron (spleen), to storage in hepatocytes, and back to TF through mobilization of iron stores. Cellular iron transport is described in detail in the text and shown in schematic form on the outside edges of this figure. (A) Nonheme iron transport across an intestinal enterocyte. (B) Erythrophagocytosis and iron recycling in a tissue macrophage. The aqua oval in the cytoplasm represents a storage depot for ferroportin protein within the cell. (C) Hepatocyte iron transport, with arrows indicating that neither import nor export is well understood. (D) Iron uptake through the transferrin cycle in the erythoblast. Illustration by Kenneth Probst.
Figure 2
Figure 2
Hepcidin and hemochromatosis. (A) The activity of hepcidin is depicted, showing ferroportin as a target both on enterocytes and macrophages. Hepcidin binds to ferroportin triggering its internalization and lysosomal degradation. (B) Three classes of hemochromatosis disorders all affect the hepcidin/ferroportin regulatory axis: Class I, defects in the hepcidin gene (HAMP) preventing production of functional hepcidin; Class II, defects in HFE, TFR2, or HFE2 genes preventing normal hepatic regulation of hepcidin expression; Class III, defects in ferroportin preventing normal regulation by hepcidin. Illustration by Kenneth Probst.

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