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
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
353-363Subventions
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.