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What regulates hepcidin in poly-transfused β-Thalassemia Major: Erythroid drive or store drive?
Author(s) -
Richa Chauhan,
Sunita Sharma,
Jagdish Chandra
Publication year - 2014
Publication title -
indian journal of pathology and microbiology/indian journal of pathology and microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.217
H-Index - 31
eISSN - 0974-5130
pISSN - 0377-4929
DOI - 10.4103/0377-4929.130891
Subject(s) - hepcidin , ferritin , soluble transferrin receptor , medicine , ineffective erythropoiesis , anemia , erythropoiesis , transferrin , thalassemia , immunology , endocrinology , iron deficiency , iron status
Hepcidin, a key regulator of iron homeostasis, is increased by iron overload and inflammation while suppressed by hypoxia. In spite of iron overload in β-Thalassemia Major (β-TM), a paradoxical decrease in hepcidin is observed.

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