PuSH - Publication Server of Helmholtz Zentrum München

Export: TXT Text RIS Endnote (RIS) BIB BibTeX
Berndt, C.* ; Alborzinia, H.* ; Amen, V.S.* ; Ayton, S.* ; Barayeu, U.* ; Bartelt, A. ; Bayir, H.* ; Bebber, C.M.* ; Birsoy, K.* ; Böttcher, J.P.* ; Brabletz, S.* ; Brabletz, T.* ; Brown, A.R.* ; Brüne, B.* ; Bulli, G.* ; Bruneau, A.* ; Chen, Q.* ; DeNicola, G.M.* ; Dick, T.P.* ; Distéfano, A.* ; Dixon, S.J.* ; Engler, J.B.* ; Esser-von Bieren, J.* ; Fedorova, M.* ; Friedmann Angeli, J.P.* ; Friese, M.A.* ; Fuhrmann, D.C.* ; García-Sáez, A.J.* ; Garbowicz, K.* ; Götz, M. ; Gu, W.* ; Hammerich, L.* ; Hassannia, B.* ; Jiang, X.* ; Jeridi, A. ; Kang, Y.P.* ; Kagan, V.E.* ; Konrad, D.B.* ; Kotschi, S.* ; Lei, P.* ; Le Tertre, M.* ; Lev, S.* ; Liang, D.* ; Linkermann, A.* ; Lohr, C.* ; Lorenz, S. ; Luedde, T.* ; Methner, A.* ; Michalke, B. ; Milton, A.V.* ; Min, J.* ; Mishima, E. ; Müller, S.* ; Motohashi, H.* ; Muckenthaler, M.U.* ; Murakami, S.* ; Olzmann, J.A.* ; Pagnussat, G.C.* ; Pan, Z.* ; Papagiannakopoulos, T.* ; Pedrera Puentes, L.* ; Pratt, D.A.* ; Proneth, B. ; Ramsauer, L.* ; Rodriguez, R.* ; Saito, Y.* ; Schmidt, F.* ; Schmitt, C.* ; Schulze, A.* ; Schwab, A.* ; Schwantes, A.* ; Soula, M.* ; Spitzlberger, B. ; Stockwell, B.R.* ; Thewes, L.* ; Thorn-Seshold, O.* ; Toyokuni, S.* ; Tonnus, W.* ; Trumpp, A.* ; Vandenabeele, P.* ; Vanden Berghe, T.* ; Venkataramani, V.* ; Vogel, F.C.E.* ; von Karstedt, S.* ; Wang, F.* ; Westermann, F.* ; Wientjens, C.* ; Wilhelm, C.* ; Wölk, M.* ; Wu, K.* ; Yang, X.* ; Yu, F.* ; Zou, Y.* ; Conrad, M.

Ferroptosis in health and disease.

Redox Biol. 75:103211 (2024)
Publ. Version/Full Text DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Ferroptosis is a pervasive non-apoptotic form of cell death highly relevant in various degenerative diseases and malignancies. The hallmark of ferroptosis is uncontrolled and overwhelming peroxidation of polyunsaturated fatty acids contained in membrane phospholipids, which eventually leads to rupture of the plasma membrane. Ferroptosis is unique in that it is essentially a spontaneous, uncatalyzed chemical process based on perturbed iron and redox homeostasis contributing to the cell death process, but that it is nonetheless modulated by many metabolic nodes that impinge on the cells' susceptibility to ferroptosis. Among the various nodes affecting ferroptosis sensitivity, several have emerged as promising candidates for pharmacological intervention, rendering ferroptosis-related proteins attractive targets for the treatment of numerous currently incurable diseases. Herein, the current members of a Germany-wide research consortium focusing on ferroptosis research, as well as key external experts in ferroptosis who have made seminal contributions to this rapidly growing and exciting field of research, have gathered to provide a comprehensive, state-of-the-art review on ferroptosis. Specific topics include: basic mechanisms, in vivo relevance, specialized methodologies, chemical and pharmacological tools, and the potential contribution of ferroptosis to disease etiopathology and progression. We hope that this article will not only provide established scientists and newcomers to the field with an overview of the multiple facets of ferroptosis, but also encourage additional efforts to characterize further molecular pathways modulating ferroptosis, with the ultimate goal to develop novel pharmacotherapies to tackle the various diseases associated with - or caused by - ferroptosis.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Altmetric
10.700
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 Review
Keywords Cancer ; Cell Death ; Iron ; Ischemia/reperfusion ; Lipid Peroxidation ; Neurodegeneration; Glutathione-peroxidase 4; Oxidative Glutamate Toxicity; Polyunsaturated Fatty-acids; Cell-death Recommendations; Oxygen Species Production; Measuring Reactive Oxygen; Persister Cancer-cells; Gtp-cyclohydrolase-i; Transfer-rna Gene; Lipid-peroxidation
Language english
Publication Year 2024
HGF-reported in Year 2024
ISSN (print) / ISBN 2213-2317
e-ISSN 2213-2317
Journal Redox Biology
Quellenangaben Volume: 75, Issue: , Pages: , Article Number: 103211 Supplement: ,
Publisher Elsevier
Publishing Place Amsterdam [u.a.]
Reviewing status Peer reviewed
Institute(s) Institute of Metabolism and Cell Death (MCD)
Institute of Diabetes and Cancer (IDC)
Institute of Stem Cell Research (ISF)
Institute of Lung Health and Immunity (LHI)
Research Unit BioGeoChemistry and Analytics (BGC)
Institute for Allergy Research (IAF)
POF-Topic(s) 30203 - Molecular Targets and Therapies
90000 - German Center for Diabetes Research
30204 - Cell Programming and Repair
30202 - Environmental Health
Research field(s) Genetics and Epidemiology
Helmholtz Diabetes Center
Stem Cell and Neuroscience
Lung Research
Environmental Sciences
Allergy
PSP Element(s) G-506900-001
G-501900-251
G-500800-001
G-505000-007
G-504800-002
G-505400-001
Grants DFG (German Research Foundation)
NIH
NSERC
DFG projects Germany's Excellence Strategy
German Federal Ministry of Education and Research (BMBF) FERROPATH
Fonds der chemischen Industrie, Physician Scientist Program of the Medical Faculty Heidelberg
SMWK
German Cancer Research Center (DKFZ)
Helmholtz Center, Consortium of excellence at University of Antwerp INFLA-MED
EU
ERC
Industrial Research Fund
BOF-IMPULS from University of Antwerp, Foundation against cancer
GIGG consortia
VIB
American Cancer Society
Bakar Fellows Spark Award
Ministry of Science & Technology of the State of Israel
Israel Science Foundation
JST CREST
JSPS Kakenhi
National Research Foundation of Korea
Seoul National University
CRIG
Special Research Fund UGent
Charcot Foundation
VLIRUOS
Research Foundation Flanders
EOS CD-INFLADIS
National Natural Science Foundation of China
DOI 10.1016/j.redox.2024.103211
WOS ID 001272568400001
Scopus ID 85196486003
PubMed ID 38908072
Erfassungsdatum 2024-06-26
[➜Report correction]