The DOI matches its Crossref record; 28 of the 28 references it cites were found in a registry or an index.
Mechanisms of Cell Death in Oxidative Stress
Abstract
Reactive oxygen or nitrogen species (ROS/RNS) generated endogenously or in response to environmental stress have long been implicated in tissue injury in the context of a variety of disease states. ROS/RNS can cause cell death by nonphysiological (necrotic) or regulated pathways (apoptotic). The mechanisms by which ROS/RNS cause or regulate apoptosis typically include receptor activation, caspase activation, Bcl-2 family proteins, and mitochondrial dysfunction. Various protein kinase activities, including mitogen-activated protein kinases, protein kinases-B/C, inhibitor-of-I-kappaB kinases, and their corresponding phosphatases modulate the apoptotic program depending on cellular context. Recently, lipid-derived mediators have emerged as potential intermediates in the apoptosis pathway triggered by oxidants. Cell death mechanisms have been studied across a broad spectrum of models of oxidative stress, including H2O2, nitric oxide and derivatives, endotoxin-induced inflammation, photodynamic therapy, ultraviolet-A and ionizing radiations, and cigarette smoke. Additionally ROS generated in the lung and other organs as the result of high oxygen therapy or ischemia/reperfusion can stimulate cell death pathways associated with tissue damage. Cells have evolved numerous survival pathways to counter proapoptotic stimuli, which include activation of stress-related protein responses. Among these, the heme oxygenase-1/carbon monoxide system has emerged as a major intracellular antiapoptotic mechanism.
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Cites
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Mammalian thioredoxin is a direct inhibitor of apoptosis signal‐regulating kinase (ASK) 1
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Cytochrome c acts as a cardiolipin oxygenase required for release of proapoptotic factors
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Carbon Monoxide Generated by Heme Oxygenase 1 Suppresses Endothelial Cell Apoptosis
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Self-citation
Cited by
Oxyl radicals, redox-sensitive signalling cascades and antioxidants
Genestra, M. (2007) · Cellular Signalling · doi:10.1016/j.cellsig.2007.04.009 · Cited by 4,930
Reactive oxygen species, cellular redox systems, and apoptosis
Circu, M. L., & Aw, T. Y. (2010) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2009.12.022 · Cited by 3,340
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Drug-induced oxidative stress and toxicity
Deavall, D. G., Martin, E. A., Horner, J. M., & Roberts, R. (2012) · Journal of Toxicology · doi:10.1155/2012/645460 · Cited by 689
Kell, D. B. (2009) · BMC Medical Genomics · doi:10.1186/1755-8794-2-2 · Cited by 554
Metadata
- Authors
- Ryter, S. W., Kim, H. P., Hoetzel, A., Park, J. W., Nakahira, K., Wang, X., & Choi, A. M. K.
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2007-01
- Volume
- 9
- Issue
- 1
- Pages
- 49-89
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- OpenAlex
- W1982460960
- Cited by
- 1,261
- References
- 28
- FWCI
- 14.37
- Type
- journal article
- Language
- en
- Open access
- closed
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