Functional consequence of Iron dyshomeostasis and ferroptosis in systemic lupus erythematosus and lupus nephritis

Copyright © 2024 Elsevier Inc. All rights reserved.

Détails bibliographiques
Publié dans:Clinical immunology (Orlando, Fla.). - 1999. - 262(2024) vom: 07. Mai, Seite 110181
Auteur principal: Morel, Laurence (Auteur)
Autres auteurs: Scindia, Yogesh
Format: Article en ligne
Langue:English
Publié: 2024
Accès à la collection:Clinical immunology (Orlando, Fla.)
Sujets:Journal Article Review Ferroptosis Iron Lupus nephritis SLE Proteins
Description
Résumé:Copyright © 2024 Elsevier Inc. All rights reserved.
Systemic lupus erythematosus (SLE) and its renal manifestation Lupus nephritis (LN) are characterized by a dysregulated immune system, autoantibodies, and injury to the renal parenchyma. Iron accumulation and ferroptosis in the immune effectors and renal tubules are recently identified pathological features in SLE and LN. Ferroptosis is an iron dependent non-apoptotic form of regulated cell death and ferroptosis inhibitors have improved disease outcomes in murine models of SLE, identifying it as a novel druggable target. In this review, we discuss novel mechanisms by which iron accumulation and ferroptosis perpetuate immune cell mediated pathology in SLE/LN. We highlight intra-renal dysregulation of iron metabolism and ferroptosis as an underlying pathogenic mechanism of renal tubular injury. The basic concepts of iron biology and ferroptosis are also discussed to expose the links between iron, cell metabolism and ferroptosis, that identify intracellular pro-ferroptotic enzymes and their protein conjugates as potential targets to improve SLE/LN outcomes
Description:Date Completed 15.04.2024
Date Revised 04.01.2025
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2024.110181