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Presented for research literature review only Siddiqui A et al
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Its core proposed mechanism is the sequestering of G-actin, which influences the cell migration central to tissue repair, alongside preclinical links to angiogenesis and reduced inflammation
[13] These intestinal lining cells can then either store the iron as ferritin, which is accomplished by Fe 2+ binding to apoferritin (in which case the iron will leave the body when the cell dies and is sloughed off into feces), or the cell can release it into the body via the only known iron exporter in mammals, ferroportin
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