Iron metabolism and erythropoiesis are closely intertwined. Erythroid precursors communicate their iron needs by modulating production of hepcidin. Under conditions of low iron absorption or altered iron metabolism, red cells production is severely impaired. In contrast, iron absorption is dramatically increased if red cell production is in high demand. In many unrelated conditions associated with inflammation and anemia, the role of several cytokines such as IL-6 and hepcidin is being recognized as the common denominator in perturbing iron metabolism and red cell production. In other disorders associated with ineffective erythropoiesis, such as beta-thalassemia and myelodysplastic syndromes (MDSs), low levels of hepcidin can increase iron absorption leading to production of nontransferrin iron bound (NTBI) and toxic organ iron overload. NTBI, in turn, can lead to increased concentration of reactive oxygen species (ROSs) that might further impair erythropoiesis. However, thalassemia and MDS might exhibit diverse manifestations in iron overload, as indicated by specific organ damage and, potentially, requiring different treatments. The mechanism by which erythroid cells modulate iron absorption is still unclear though many recent discoveries in the field of iron metabolism rejuvenated this field. Bone morphogenetic proteins (BMPs) play a major role in setting the baseline hepcidin level in collaboration with the hemochromatosis-related proteins hemojuvelin, HFE, transferrin receptor 2, and other transcriptional factors and proteases that control their synthesis or posttranslational activity, such as Smad 4, furin, or TMPRSS6. Under condition of ineffective erythropoiesis, hepcidin can be downmodulated factors secreted by erythroid cells named GDF-15 and TWSG1. In anemias, regulation of hepcidin might also be mediated by erythropoietin and hypoxia.

We invite authors to present original articles as well as review articles that will stimulate the continuing efforts in defining the role of proteins that control iron demand. We are particularly interested in those proteins that, while modulating iron metabolism, have a strong impact, directly or indirectly, on erythropoiesis. Basic research articles and reviews covering the subject of erythropoiesis and iron metabolism and manuscripts that describe the state of the art in the clinical care to prevent the damage due to altered iron absorption are welcomed.

Potential topics include but are not limited to:

• Erythropoiesis and iron metabolism
• Hepcidin in disorders of iron and erythropoiesis
• Inflammation, iron, and anemia
• The labile iron pool, ROS, and erythropoiesis
• Iron metabolism in disorders associate with altered erythropoiesis, such as beta-thalassemia, MDS, and polycythemia vera
• Progress in iron chelation and management of hemoglobinopathies

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/ah/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/ according to the following timetable: