期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 133, 期 -, 页码 144-152出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2018.09.014
关键词
Regulated necrosis; GPX4; Lipid peroxidation; Cysteine metabolism; Non-apoptotic cell death; Ferritinophagy
资金
- FoFoLe program by Ludwig-Maximilians-Universitat Munchen
- Deutsche Forschungsgemeinschaft (DFG) [CO 291/5-2]
- Human Frontier Science Program (HFSP) [RGP0013]
- Helmholtz Validation Funds (Helmholtz Association of German Research Centres)
- German Federal Ministry of Education and Research (BMBF) through the Joint Project Modelling ALS Disease In Vitro (MAIV) [01EK1611B]
- VIP + program NEUROPROTEKT [03VP04260]
Ferroptosis is a non-apoptotic form of cell death characterized by iron-dependent lipid peroxidation and metabolic constraints. Dependence on NADPH/H+, polyunsaturated fatty acid metabolism, and the mevalonate and glutaminolysis metabolic pathways have been implicated in this novel form of regulated necrotic cell death. Genetic studies performed in cells and mice established the selenoenzyme glutathione peroxidase (GPX4) as the key regulator of this form of cell death. Besides these genetic models, the identification of a series of small molecule ferroptosis-specific inhibitors and inducers have not only helped in the delineation of the molecular underpinnings of ferroptosis but they might also prove highly beneficial when tipping the balance between cell death inhibition and induction in the context of degenerative diseases and cancer, respectively. In the latter, the recent recognition that a subset of cancer cell lines including certain triple negative breast cancer cells and those of therapy-resistant high-mesenchymal cell state present a high dependence on this lipid make-up offers unprecedented opportunities to eradicate difficult to treat cancers. Due to the rapidly growing interest in this form of cell death, we provide an overview herein what we know about this field today and its future translational impact.
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