Zhao You-Shan, Chang Chun-Kang
Department of Hematology, Shanghai Jiaotong University, Shanghai 200233, China.
Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2011 Apr;19(2):537-41.
Ineffective erythropoiesis is recognized as the principal reason of non-transfusional iron overload. In the process of expanded erythropoiesis, the apoptosis of erythroblasts induces the up-regulation of GDF15. GDF15 suppresses hepcidin production by the hepatocytes. Subsequently, low hepcidin levels increase iron absorption from the intestine resulting in iron overload. Physiological dose of GDF15 can promote the growth and differentiation of erythroid progenitors, but the high dose of GDF15 can suppress the secretion of hepcidin. The regulation of GDF15 may also be related to iron levels, epigenetic regulation and hypoxia. In this article the GDF15 and its expression and distribution, roles of GDF15 in erythropoiesis and iron overload, as well as the regulation factors of GDF15 are reviewed.
无效红细胞生成被认为是非输血性铁过载的主要原因。在红细胞生成增加的过程中，成红细胞的凋亡诱导生长分化因子15（GDF15）上调。GDF15抑制肝细胞生成铁调素。随后，低水平的铁调素会增加肠道对铁的吸收，从而导致铁过载。生理剂量的GDF15可促进红系祖细胞的生长和分化，但高剂量的GDF15会抑制铁调素的分泌。GDF15的调节也可能与铁水平、表观遗传调节和缺氧有关。本文对GDF15及其表达和分布、GDF15在红细胞生成和铁过载中的作用以及GDF15的调节因子进行综述。
