| Literature DB >> 29699840 |
Alessandro Isidori1, Lorenza Borin2, Elena Elli3, Roberto Latagliata4, Bruno Martino5, Giuseppe Palumbo6, Federica Pilo7, Federica Loscocco8, Giuseppe Visani9, Paolo Cianciulli10.
Abstract
Excess iron can be extremely toxic for the body and may cause organ damage in the absence of iron chelation therapy. Preclinical studies on the role of free iron on bone marrow function have shown that iron toxicity leads to the accumulation of reactive oxygen species, affects the expression of genes coding for proteins that regulate hematopoiesis, and disrupts hematopoiesis. These effects could be partially attenuated by iron-chelation treatment with deferasirox, suggesting iron toxicity may have a negative impact on the hematopoietic microenvironment. Iron toxicity is of concern in transfusion-dependent patients. Importantly, iron chelation with deferasirox can cause the loss of transfusion dependency and may induce hematological responses, although the mechanisms through which deferasirox exerts this action are currently unknown. This review will focus on the possible mechanisms of toxicity of free iron at the bone marrow level and in the bone marrow microenvironment.Entities:
Keywords: Aplastic anemia; Bone marrow microenvironment; Hematopoietic stem cell transplantation; Iron chelation; Iron toxicity; Myelodysplastic syndrome; Myelofibrosis
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Year: 2018 PMID: 29699840 DOI: 10.1016/j.blre.2018.04.004
Source DB: PubMed Journal: Blood Rev ISSN: 0268-960X Impact factor: 8.250