The DOI matches its Crossref record; 272 of the 272 references it cites were found in a registry or an index.
Oxidative cell death in cancer: mechanisms and therapeutic opportunities
Open accessAbstract
Reactive oxygen species (ROS) are highly reactive oxygen-containing molecules generated as natural byproducts during cellular processes, including metabolism. Under normal conditions, ROS play crucial roles in diverse cellular functions, including cell signaling and immune responses. However, a disturbance in the balance between ROS production and cellular antioxidant defenses can lead to an excessive ROS buildup, causing oxidative stress. This stress damages essential cellular components, including lipids, proteins, and DNA, potentially culminating in oxidative cell death. This form of cell death can take various forms, such as ferroptosis, apoptosis, necroptosis, pyroptosis, paraptosis, parthanatos, and oxeiptosis, each displaying distinct genetic, biochemical, and signaling characteristics. The investigation of oxidative cell death holds promise for the development of pharmacological agents that are used to prevent tumorigenesis or treat established cancer. Specifically, targeting key antioxidant proteins, such as SLC7A11, GCLC, GPX4, TXN, and TXNRD, represents an emerging approach for inducing oxidative cell death in cancer cells. This review provides a comprehensive summary of recent progress, opportunities, and challenges in targeting oxidative cell death for cancer therapy.
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1 retracted
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Self-citationRetractedFerroptosis: An Iron-Dependent Form of Nonapoptotic Cell Death
Dixon, S. J., Lemberg, K. M., Lamprecht, M. R., Skouta, R., Zaitsev, E. M., Gleason, C. E., Patel, D. N., Bauer, A. J., Cantley, A. M., Yang, W. S., et al. (2012) · Cell · doi:10.1016/j.cell.2012.03.042 · Cited by 18,691
Free radicals and antioxidants in normal physiological functions and human disease
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Reactive oxygen species: Metabolism, oxidative stress, and signal transduction
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Regulation of Ferroptotic Cancer Cell Death by GPX4
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Self-citationMitochondrial Reactive Oxygen Species (ROS) and ROS-Induced ROS Release
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Reactive oxygen species (ROS) as pleiotropic physiological signalling agents
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Copper induces cell death by targeting lipoylated TCA cycle proteins
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Metadata
- Authors
- An, X., Yu, W., Liu, J., Tang, D., Yang, L., & Chen, X.
- Venue
- Cell Death & Disease
- Published
- 2024-08-01
- Volume
- 15
- Issue
- 8
- Pages
- 556-556
- ISSN
- 2041-4889 (ISSN-L)
- OpenAlex
- W4401211263
- Cited by
- 523
- References
- 272
- FWCI
- 60.77
- Type
- journal article
- Language
- en
- Open access
- gold
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.