The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Redox Control of Cell Death
Abstract
Cellular redox is controlled by the thioredoxin (Trx) and glutathione (GSH) systems that scavenge harmful intracellular reactive oxygen species (ROS). Oxidative stress also evokes many intracellular events including apoptosis. There are two major pathways through which apoptosis is induced; one involves death receptors and is exemplified by Fas-mediated caspase-8 activation, and another is the stress- or mitochondria-mediated caspase-9 activation pathway. Both pathways converge on caspase-3 activation, resulting in nuclear degradation and cellular morphological change. Oxidative stress induces cytochrome c release from mitochondria and activation of caspases, p53, and kinases, including apoptosis signal-regulating kinase 1 (ASK1), c-Jun N-terminal kinase, and p38 mitogen-activated protein kinase. Trx inhibits apoptosis signaling not only by scavenging intracellular ROS in cooperation with the GSH system, but also by inhibiting the activity of ASK1 and p38. Mitochondria-specific thioredoxin (Trx-2) and Trx peroxidases (peroxiredoxins) are suggested to regulate cytochrome c release from mitochondria, which is a critical early step in the apoptotis-signaling pathway. dATP/ATP and reducing factors including Trx determine the manifestation of cell death, apoptosis or necrosis, by regulating the activation process and the activity of redox-sensitive caspases. As mitochondria are the most redox-active organelle and indispensable for cells to initiate or inhibit the apoptosis process, the regulation of mitochondrial function is the central focus in the research field of apoptosis and redox.
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Cites
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Tumor suppressor p53 is a direct transcriptional activator of the human bax gene
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Molecular characterization of mitochondrial apoptosis-inducing factor
Susin, S. A., Lorenzo, H. K., Zamzami, N., Marzo, I., Snow, B. E., Brothers, G. M., Mangion, J., Jacotot, E., Costantini, P., Loeffler, M., et al. (1999) · Nature · doi:10.1038/17135 · Cited by 4,060
Mammalian thioredoxin is a direct inhibitor of apoptosis signal‐regulating kinase (ASK) 1
Saitoh, M., Nishitoh, H., Fujii, M., Takeda, K., Tobiume, K., Sawada, Y., Kawabata, M., Miyazono, K., & Ichijo, H. (1998) · The EMBO Journal · doi:10.1093/emboj/17.9.2596 · Cited by 2,377
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Diverse functions of JNK signaling and c-Jun in stress response and apoptosis
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Roles for p53 in growth arrest and apoptosis: putting on the brakes after genotoxic stress
Amundson, S. A., Myers, T. G., & Fornace, A. J. (1998) · Oncogene · doi:10.1038/sj.onc.1202576 · Cited by 424
Thioredoxin‐2 (TRX‐2) is an essential gene regulating mitochondria‐dependent apoptosis
Tanaka, T., Hosoi, F., Yamaguchi‐Iwai, Y., Nakamura, H., Masutani, H., Ueda, S., Nishiyama, A., Takeda, S., Wada, H., Spyrou, G., et al. (2002) · The EMBO Journal · doi:10.1093/emboj/21.7.1695 · Cited by 322 · cited 2×
“It is possible that diamide inactivates the reducing function of Trx-2 in mitochondria and induces cytochrome c release by modulating the function of VDAC or mitochondrial megachannel (80, 82).”
Self-citationCostantini, P., Belzacq, A.-S., Vieira, H. L., Larochette, N., de Pablo, M. A., Zamzami, N., Susin, S. A., Brenner, C., & Kroemer, G. (2000) · Oncogene · doi:10.1038/sj.onc.1203299 · Cited by 284
Cited by
Mitochondrial membrane permeabilization in cell death
Kroemer, G., Galluzzi, L., & Brenner, C. (2007) · Physiological Reviews · doi:10.1152/physrev.00013.2006 · Cited by 3,598
Calcium, ATP, and ROS: a mitochondrial love-hate triangle
Brookes, P. S., Yoon, Y., Robotham, J. L., Anders, M. W., & Sheu, S.-S. (2004) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00139.2004 · Cited by 2,575
Flavonoids: antioxidants or signalling molecules?
Williams, R. J., Spencer, J. P. E., & Rice-Evans, C. (2004) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2004.01.001 · Cited by 2,016
Reactive Oxygen Species: A Breath of Life or Death?
Fruehauf, J. P., & Meyskens, F. L. (2007) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-06-2082 · Cited by 915
Kregel, K. C., & Zhang, H. J. (2007) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00327.2006 · Cited by 883
Metadata
- Authors
- Ueda, S., Masutani, H., Nakamura, H., Tanaka, T., Ueno, M., & Yodoi, J.
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2002-06
- Volume
- 4
- Issue
- 3
- Pages
- 405-414
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- OpenAlex
- W1999605572
- Cited by
- 548
- References
- 9
- FWCI
- 10.69
- Type
- journal article
- Language
- en
- Open access
- closed
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