PuSH - Publication Server of Helmholtz Zentrum München

Export: TXT Text RIS Endnote (RIS) BIB BibTeX
Van San, E.* ; Debruyne, A.C.* ; Veeckmans, G.* ; Tyurina, Y.Y.* ; Tyurin, V.A.* ; Zheng, H.* ; Choi, S.M.* ; Augustyns, K.* ; van Loo, G.* ; Michalke, B. ; Venkataramani, V.* ; Toyokuni, S.* ; Bayir, H.* ; Vandenabeele, P.* ; Hassannia, B.* ; Vanden Berghe, T.*

Ferroptosis contributes to multiple sclerosis and its pharmacological targeting suppresses experimental disease progression.

Cell Death Differ. 30, 2092-2103 (2023)
Publ. Version/Full Text DOI PMC
Open Access Hybrid
Creative Commons Lizenzvertrag
Multiple sclerosis (MS) is a chronic autoimmune disorder characterized by central nervous (CNS) demyelination resulting in axonal injury and neurological deficits. Essentially, MS is driven by an auto-amplifying mechanism of inflammation and cell death. Current therapies mainly focus on disease modification by immunosuppression, while no treatment specifically focuses on controlling cell death injury. Here, we report that ferroptosis, an iron-catalyzed mode of regulated cell death (RCD), contributes to MS disease progression. Active and chronic MS lesions and cerebrospinal fluid (CSF) of MS patients revealed several signs of ferroptosis, reflected by the presence of elevated levels of (labile) iron, peroxidized phospholipids and lipid degradation products. Treatment with our candidate lead ferroptosis inhibitor, UAMC-3203, strongly delays relapse and ameliorates disease progression in a preclinical model of relapsing-remitting MS. In conclusion, the results identify ferroptosis as a detrimental and targetable factor in MS. These findings create novel treatment options for MS patients, along with current immunosuppressive strategies.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Altmetric
12.400
0.000
2
Tags
Annotations
Special Publikation
Hide on homepage

Edit extra information
Edit own tags
Private
Edit own annotation
Private
Hide on publication lists
on hompage
Mark as special
publikation
Publication type Article: Journal article
Document type Scientific Article
Keywords Experimental Autoimmune Encephalomyelitis; Lipid-peroxidation; Cell-death; B-cells; Iron; Myelin; Mice; Induction; Injury; Damage
Language english
Publication Year 2023
HGF-reported in Year 2023
ISSN (print) / ISBN 1350-9047
e-ISSN 1476-5403
Journal Cell Death and Differentiation
Quellenangaben Volume: 30, Issue: 9, Pages: 2092-2103 Article Number: , Supplement: ,
Publisher Nature Publishing Group
Publishing Place Campus, 4 Crinan St, London, N1 9xw, England
Reviewing status Peer reviewed
Institute(s) Research Unit BioGeoChemistry and Analytics (BGC)
POF-Topic(s) 30202 - Environmental Health
Research field(s) Environmental Sciences
PSP Element(s) G-504800-002
Grants Excellence of Science MODEL-IDI
CD-INFLADIS
~Consortium of excellence at University of Antwerp INFLA-MED
Industrial Research Fund
BOF-IMPULS from University of Antwerp
Research Foundation Flanders
Foundation against cancer
Charcot Foundation
VLIRUOS
FWO
Flemish Institute of Biotechnology VIB
iBOF ATLANTIS
CRIG
GIGG consortia
NIH
DOI 10.1038/s41418-023-01195-0
WOS ID 001043074400001
Scopus ID 85166776734
PubMed ID 37542104
Erfassungsdatum 2023-10-06
[➜Report correction]