Ganz Figure 2.
Ganz Figure 2. Regulation of systemic iron flows in normal subjects (A), patients with hereditary hemochromatosis (B) and patients with anemia of inflammation (C). / Iron flows are depicted by blue arrows and the effect of hepcidin by red arrows. Hepcidin-mediated regulation of iron efflux through ferroportin is depicted by valves that variably restrict iron flows. When hepcidin is deficient (B), iron absorption in the duodenum is increased, plasma transferrin becomes saturated with iron, and excess iron flows into the liver (large dark blue arrows). In anemia of inflammation (C), hepcidin synthesis is stimulated by inflammatory cytokines, and increased hepcidin (large red arrows) blocks major iron flows into plasma (light blue arrows). Plasma iron is decreased, limiting erythropoiesis.

Regulation of systemic iron flows in normal subjects (A), patients with hereditary hemochromatosis (B) and patients with anemia of inflammation (C).

Iron flows are depicted by blue arrows and the effect of hepcidin by red arrows. Hepcidin-mediated regulation of iron efflux through ferroportin is depicted by valves that variably restrict iron flows. When hepcidin is deficient (B), iron absorption in the duodenum is increased, plasma transferrin becomes saturated with iron, and excess iron flows into the liver (large dark blue arrows). In anemia of inflammation (C), hepcidin synthesis is stimulated by inflammatory cytokines, and increased hepcidin (large red arrows) blocks major iron flows into plasma (light blue arrows). Plasma iron is decreased, limiting erythropoiesis.

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