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Nutritional and metabolic control of ferroptosis.

Ann. Rev. Nutr. 42, 275-309 (2022)
Verlagsversion DOI PMC
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Open Access Green: Postprint online verfügbar 07/2023
Ferroptosis is a type of regulated cell death characterized by an excessive lipid peroxidation of cellular membranes caused by the disruption of the antioxidant defense system and/or an imbalanced cellular metabolism. Ferroptosis differentiates from other forms of regulated cell death in that several metabolic pathways and nutritional aspects, including endogenous antioxidants (such as coenzyme Q10, vitamin E, and di/tetrahydrobiopterin), iron handling, energy sensing, selenium utilization, amino acids, and fatty acids, directly regulate the cells' sensitivity to lipid peroxidation and ferroptosis. As hallmarks of ferroptosis have been documented in a variety of diseases, including neurodegeneration, acute organ injury, and therapy-resistant tumors, the modulation of ferroptosis using pharmacological tools or by metabolic reprogramming holds great potential for the treatment of ferroptosis-associated diseases and cancer therapy. Hence, this review focuses on the regulation of ferroptosis by metabolic and nutritional cues and discusses the potential of nutritional interventions for therapy by targeting ferroptosis. Expected final online publication date for the Annual Review of Nutrition, Volume 42 is August 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Sprache englisch
Veröffentlichungsjahr 2022
HGF-Berichtsjahr 2022
ISSN (print) / ISBN 0199-9885
e-ISSN 1545-4312
Quellenangaben Band: 42, Heft: , Seiten: 275-309 Artikelnummer: , Supplement: ,
Verlag Annual Reviews
Verlagsort Palo Alto, Calif.
Begutachtungsstatus Peer reviewed
POF Topic(s) 30203 - Molecular Targets and Therapies
Forschungsfeld(er) Genetics and Epidemiology
PSP-Element(e) G-506900-001
Förderungen Bundesministerium für Bildung und Forschung
Japan Society for the Promotion of Science
Deutsche Forschungsgemeinschaft
European Research Council
Uehara Memorial Foundation
Watanabe Foundation
Japan Heart Foundation/Bayer Yakuhin
Horizon 2020
PubMed ID 35650671
Erfassungsdatum 2022-07-11