Pathogenic Mechanisms in Thalassemia II: Iron Overload

Tomas Ganz; Elizabeta Nemeth

doi:10.1016/j.hoc.2022.12.006

Pathogenic Mechanisms in Thalassemia II: Iron Overload

Hematol Oncol Clin North Am. 2023 Apr;37(2):353-363. doi: 10.1016/j.hoc.2022.12.006.

Authors

Tomas Ganz¹, Elizabeta Nemeth²

Affiliations

¹ Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1690, USA. Electronic address: tganz@mednet.ucla.edu.
² Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1690, USA.

PMID: 36907608
DOI: 10.1016/j.hoc.2022.12.006

Abstract

Iron overload remains a lethal complication of β-thalassemia and other anemias caused by ineffective erythropoiesis. This review discusses the pathogenetic mechanisms of iron overload in thalassemia, at organismal, cellular, and molecular levels.

Keywords: Erythroferrone; Hepcidin; Ineffective erythropoiesis; Nontransferrin-bound iron.

Publication types

Review
Research Support, N.I.H., Extramural

MeSH terms

Erythropoiesis
Hepcidins
Humans
Iron Overload* / etiology
Thalassemia* / complications
beta-Thalassemia*

Substances

Hepcidins

Grants and funding

R01 DK126680/DK/NIDDK NIH HHS/United States