Hepcidin- interesa para los anémicos

Hepcidin, a mainly liver-derived antimicrobial acute phase protein, reduces both duodenal iron absorption and iron release from macrophages. These effects can be explained by the interaction of hepcidin and the transmembrane protein ferroportin, the only so far known iron exporter in mammalians  

In macrophages, which have a general turnover of ∼20 to 25 mg of iron per day as a result of being recycled from senescent red blood cells (RBCs), this produces iron restriction with an accompanying increase in ferritin levels and decrease in transferrin saturation (TSAT), resulting in a relative iron-deficient erythropoiesis.

Increased hepcidin levels have been reported in cancer patients and patients suffering from autoimmune disease and CKD. Remarkably, elevated hepcidin levels have also been reported in older patients, with an age-related increase. 

 As hepcidin seems to be the central player in iron metabolism, several mechanisms are involved in tightly controlling hepcidin. Hepcidin expression is upregulated by inflammatory cytokines like IL-6 and different bone morphogenic proteins (BMPs), mainly BMP6 .
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Thanks to a better understanding of mechanisms regulating erythropoiesis, new drugs are currently being developed such as hepcidin inhibitors. Currently, these drugs are mainly developed for anemia in CKD and cancer patients. However, they may be a future therapeutic approach for a defined group of elderly patients.

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