Kattamis Antonis, Papassotiriou Ioannis, Palaiologou Danai, Apostolakou Filia, Galani Angeliki, Ladis Vassilis, Sakellaropoulos Nikos, Papanikolaou George
First Department of Pediatrics, National and Kapodistrian University of Athens Medical School, Athens 11527, Greece.
Haematologica. 2006 Jun;91(6):809-12.
Hepcidin production is homeostatically regulated by iron stores, anemia and hypoxia. We evaluated the effect of iron overload and of ineffective erythropoeisis on hepcidin expression in patients with thalassemia major. Liver hepcidin mRNA levels correlated with hemoglobin concentration and inversely correlated with serum transferrin receptor, erythropoietin and non-transferrin-bound iron. They did not correlate with indices of iron load. Urinary hepcidin levels were disproportionably suppressed in regards to iron burden. We conclude that hepcidin expression is regulated mainly by increased erythropoietic activity rather than by iron load and that hepcidin plays a central regulatory role in iron circulation and iron toxicity in patients with thalassemia.
铁调素的产生通过铁储备、贫血和缺氧进行稳态调节。我们评估了铁过载和无效红细胞生成对重型地中海贫血患者铁调素表达的影响。肝脏铁调素mRNA水平与血红蛋白浓度相关，与血清转铁蛋白受体、促红细胞生成素和非转铁蛋白结合铁呈负相关。它们与铁负荷指标无关。尿铁调素水平相对于铁负荷被不成比例地抑制。我们得出结论，铁调素的表达主要受红细胞生成活性增加的调节，而非铁负荷，并且铁调素在重型地中海贫血患者的铁循环和铁毒性中起核心调节作用。
