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Hepatocellular Iron Uptake and Storage

Hepatocellular iron uptake is especially efficient, owing to the high number of transferrin receptors on the cell surface. When liver iron storage reaches critical levels, non-transferrin-bound iron (NTBI) is released from endosomes into intracellular labile iron pools, and begins to attack cellular organelles such as mitochondria, producing damage that can lead to cellular dysfunction and death. In response to increased intracellular iron levels, the liver synthesizes and releases hepcidin, which has a dual role — it stimulates increased iron storage by reticuloendothelial macrophages, (1) and decreases iron absorption by enterocytes (2).

Hepatocellular iron uptake and storage mechanisms

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Transferrin

Ferritin

Ferroportin

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Iron and Hepatic Damage

The development of liver fibrosis
directly correlates
to liver iron concentrations and serum ferritin levels.

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