Pathogenic Mechanisms in Thalassemia II: Iron Overload.

Erythroferrone Hepcidin Ineffective erythropoiesis Nontransferrin-bound iron

Journal

Hematology/oncology clinics of North America
ISSN: 1558-1977
Titre abrégé: Hematol Oncol Clin North Am
Pays: United States
ID NLM: 8709473

Informations de publication

Date de publication:
04 2023
Historique:
entrez: 12 3 2023
pubmed: 13 3 2023
medline: 15 3 2023
Statut: ppublish

Résumé

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.

Identifiants

pubmed: 36907608
pii: S0889-8588(22)00147-2
doi: 10.1016/j.hoc.2022.12.006
pii:
doi:

Substances chimiques

Hepcidins 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

353-363

Subventions

Organisme : NIDDK NIH HHS
ID : R01 DK126680
Pays : United States

Informations de copyright

Copyright © 2022 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Disclosure T. Ganz and E. Nemeth are shareholders in Intrinsic LifeSciences and Silarus Pharma, and have received consulting fees from Disc Medicine, FibrogenAstraZeneca, Ionis Pharmaceuticals, and Rallybio. T. Ganz has also received consulting fees from Alnylam Pharmaceuticals, Akebia Therapeutics, Global Blood Therapeutics, Gossamer Bio, Pharmacosmos, Sierra Oncology and Silence Therapeutics, Elizabeta Nemeth from GSK, Novo Nordisk, Protagonist, and Shield Therapeutics.

Auteurs

Tomas Ganz (T)

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

Elizabeta Nemeth (E)

Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1690, USA.

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Classifications MeSH