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Paradoxically, Hepc levels can be decreased in β thalassemia-mediated cardiomyopathy as well as other iron overload-mediated conditions, where erythropoiesis-dependent downregulation of Hepc should prevail and these low levels of circulating Hepc are believed partially responsible for the ferroportin 1 expression and export activity, thereby concurring to limit iron accumulation in the heart [25]
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