The DOI matches its OpenAlex record; 17 of the 17 references it cites were found in a registry or an index.
Reactive oxygen species and the mitochondrial signaling pathway of cell death.
Open accessAbstract
Reactive oxygen species (ROS) are produced as a by-product of cellular metabolic pathways and function as a critical second messenger in a variety of intracellular signaling pathways. Thus, a defect or deficiency in the anti-oxidant defense system on the one hand and/or the excessive intracellular generation of ROS on the other renders a cell oxidatively stressed. As a consequence, direct or indirect involvement of ROS in numerous diseases has been documented. In most of these cases, the deleterious effect of ROS is a function of activation of intracellular cell-death circuitry. To that end, involvement of ROS at different phases of the apoptotic pathway, such as induction of mitochondrial permeability transition and release of mitochondrial death amplification factors, activation of intracellular caspases and DNA damage, has been clearly established. For instance, the ROS-induced alteration of constitutive mitochondrial proteins, such as the voltage-dependent anion channel (VDAC) and/or the adenine nucleotide translocase (ANT) can induce the pro-apoptotic mitochondrial membrane permabilization. Not only do these observations provide insight into the intricate mechanisms underlying a variety of disease states, but they also present novel opportunities for the design and development of more effective therapeutic strategies.
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Citations
Cites
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Reactive Oxygen Species (Ros-Induced) Ros Release
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Self-citationVDAC2 Inhibits BAK Activation and Mitochondrial Apoptosis
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Cited by
Redox regulation of cell survival
Trachootham, D., Lu, W., Ogasawara, M. A., Valle, N. R.-D., & Huang, P. (2008) · Antioxidants & Redox Signaling · doi:10.1089/ars.2007.1957 · Cited by 1,781
Reactive Oxygen Species: A Breath of Life or Death?
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Mitochondria-Ros Crosstalk in the Control of Cell Death and Aging
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Metadata
- Authors
- Bras, M. L., Clément, M.-V., Pervaiz, S., & Brenner, C.
- Venue
- PubMed
- Publisher
- National Institutes of Health
- Published
- 2005-01-01
- Volume
- 20
- Issue
- 1
- Pages
- 205-19
- OpenAlex
- W49470374
- Cited by
- 359
- References
- 17
- FWCI
- 7.95
- Type
- journal article
- Language
- en
- Open access
- green
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