By Gunter Weiss, Victor R. Gordeuk, Chaim Hershko
This publication summarizes the most up-tp-date examine at the anemia of power disorder and identifies powerful diagnostic recommendations for this universal scientific condition-covering key issues concerning the layout and choice of healing innovations together with the therapy of the underlying ailment, the biology of erythropoietin and the law of erythropoiesis, the disturbance of iron homeostasis, and the advanced nature of the systemic inflammatory reaction.
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Additional resources for Anemia of Chronic Disease (Basic and Clinical Oncology)
Taken together, these data have established a function of hepcidin as a novel iron-regulatory humoral factor controlling dietary iron absorption and utilization for erythropoiesis (Fig. 6). On the basis of the above findings, it can be easily predicted that misregulation of hepcidin expression would associate with disease. Several lines of evidence support this view. First, increased hepcidin expression was found in hepatic adenoma tissue from patients with glycogen storage disease that had developed severe iron refractory anemia (101).
Interestingly, mice lacking expression of either b2-microglobulin (34–36) or classical MHC class I molecules (37) also develop iron overload. Additional disorders of hereditary iron overload include juvenile hemochromatosis (HH of type 2) (38), HH of types 3, 4, and 5 (26,39), neonatal hemochromatosis (40), African iron overload (41), aceruloplasminemia (42), hypotransferrinemia= atransferrinemia (39), and heme oxygenase 1 deficiency (39). The above disorders are rare or extremely rare, but studies on the underlying molecular mechanisms and the development of animal models (43) have provided and continue to provide valuable insights on the regulation of iron metabolism in the body.
Acidification of the endosome results in the release of ferric iron from Tf and reduction and subsequent transport of ferrous iron across the endosomal membrane by DMT1. In the cytoplasm, iron is utilized for the synthesis of iron-containing proteins and excess is stored in ferritin. The pathway is completed by recycling of the apoTf–TfR complex to the cell surface and release of apoTf. Association of TfR1 with HFE impairs the binding of extracellular diferric-Tf and negatively regulates the cycle.