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Conrad, M. ; Costa da Silva, M.*

Ferroptosis: Physiological and pathophysiological aspects.

In: Oxidative Stress: Eustress and Distress. 2020. 149-166
DOI Verlagsversion bestellen
Ferroptosis is a recently described form of regulated necrosis entirely distinct from other forms of cell death. Cysteine availability either through uptake via system xc- or the transsulfuration pathway, glutathione biosynthesis, and proper functioning of GPX4 are the core to prevent iron-dependent lipid peroxidation and ferroptosis. While the role of ferroptosis in physiological contexts remains to be clarified, its contribution to pathophysiological processes including neurodegeneration and ischemia/reperfusion injuries has been demonstrated in animal models of the disease. On the other hand, emerging evidence shows that system xc- is under the direct control of the tumor suppressors p53 and BAP1 as well as IFN-gamma derived from CD8-positive T cells. Additionally, standard therapy-resistant persister tumor cells present a high vulnerability toward ferroptosis, thus providing an Achilles’ heel for therapeutic intervention. Hence, it emerges that sensitizing tumor cells to ferroptosis via cell autonomous and nonautonomous mechanisms may present a “physiological response” to counteract (pre)malignant cells.
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Publikationstyp Artikel: Sammelbandbeitrag/Buchkapitel
Schlagwörter Cysteine Metabolism ; Eicosanoid Metabolism ; Fatty Acid Metabolism ; Glutathione ; Iron Metabolism ; Lipid Peroxidation
Bandtitel Oxidative Stress: Eustress and Distress
Quellenangaben Band: , Heft: , Seiten: 149-166 Artikelnummer: , Supplement: ,