Effect of GDF15 on iron overloading and erythropoiesis / 中国实验血液学杂志
Journal of Experimental Hematology
;
(6): 537-541, 2011.
Artigo
em Chinês
| WPRIM
| ID: wpr-313950
ABSTRACT
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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Sobrecarga de Ferro
/
Eritropoese
/
Fator 15 de Diferenciação de Crescimento
/
Metabolismo
Limite:
Humanos
Idioma:
Chinês
Revista:
Journal of Experimental Hematology
Ano de publicação:
2011
Tipo de documento:
Artigo
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