PuSH - Publication Server of Helmholtz Zentrum München

Export: TXT Text RIS Endnote (RIS) BIB BibTeX
Tschuck, J. ; Tonnus, W.* ; Gavali, S.* ; Kolak, A. ; Mallais, M.* ; Maremonti, F.* ; Sato, M.* ; Rothenaigner, I. ; Friedmann Angeli, J.P.* ; Pratt, D.A.* ; Linkermann, A.* ; Hadian, K.

Seratrodast inhibits ferroptosis by suppressing lipid peroxidation.

Cell Death Dis. 15:853 (2024)
Publ. Version/Full Text DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Ferroptosis is a regulated and non-apoptotic form of cell death mediated by iron-dependent peroxidation of polyunsaturated fatty acyl tails in phospholipids. Research of the past years has shed light on the occurrence of ferroptosis in organ injury and degenerative diseases of the brain, kidney, heart, and other tissues. Hence, ferroptosis inhibition may prove therapeutically beneficial to treat distinct diseases. In this study, we explored the ferroptosis-modulating activity of seratrodast, an inhibitor of thromboxane A2 (TXA2) receptor, which is approved in some countries for the treatment of asthma. Interestingly, seratrodast suppressed ferroptosis, but not apoptosis and necroptosis; thus, demonstrating selective anti-ferroptotic activity. While seratrodast itself does not inhibit lipid peroxidation, it exhibits potent radical-trapping antioxidant activity upon reduction to its corresponding hydroquinone form-analogously to ubiquinone and vitamin K. Importantly, seratrodast ameliorated the severity of renal ischemia-reperfusion injury in mice. Together, this study provides a drug repurposing case, where seratrodast-a marketed drug-can undergo fast-forward preclinical/clinical development for the inhibition of ferroptosis in distinct degenerative diseases.
Impact Factor
Scopus SNIP
Altmetric
8.100
0.000
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 Cell-death; Reactivity; Mechanisms
Language english
Publication Year 2024
HGF-reported in Year 2024
ISSN (print) / ISBN 2041-4889
e-ISSN 2041-4889
Journal Cell Death & Disease
Quellenangaben Volume: 15, Issue: 11, Pages: , Article Number: 853 Supplement: ,
Publisher Nature Publishing Group
Publishing Place Campus, 4 Crinan St, London, N1 9xw, England
Reviewing status Peer reviewed
Institute(s) Research Unit Signaling and Translation (SAT)
POF-Topic(s) 30203 - Molecular Targets and Therapies
Research field(s) Enabling and Novel Technologies
PSP Element(s) G-509800-003
Grants Helmholtz Munich
Projekt DEAL
natural sciences and engineering research council of canada
DOI 10.1038/s41419-024-07251-y
WOS ID 001361307900002
Scopus ID 85209765702
PubMed ID 39578434
Erfassungsdatum 2024-12-02
[➜Report correction]