Redox regulation of cell survival.
Journal: 2008/September - Antioxidants and Redox Signaling
ISSN: 1557-7716
Abstract:
Reactive oxygen species (ROS) and reactive nitrogen species (RNS) play important roles in regulation of cell survival. In general, moderate levels of ROS/RNS may function as signals to promote cell proliferation and survival, whereas severe increase of ROS/RNS can induce cell death. Under physiologic conditions, the balance between generation and elimination of ROS/RNS maintains the proper function of redox-sensitive signaling proteins. Normally, the redox homeostasis ensures that the cells respond properly to endogenous and exogenous stimuli. However, when the redox homeostasis is disturbed, oxidative stress may lead to aberrant cell death and contribute to disease development. This review focuses on the roles of key transcription factors, signal-transduction pathways, and cell-death regulators in affecting cell survival, and how the redox systems regulate the functions of these molecules. The current understanding of how disturbance in redox homeostasis may affect cell death and contribute to the development of diseases such as cancer and degenerative disorders is reviewed. We also discuss how the basic knowledge on redox regulation of cell survival can be used to develop strategies for the treatment or prevention of those diseases.
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Antioxid Redox Signal 10(8): 1343-1374

Redox Regulation of Cell Survival

Department of Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, Texas.
Faculty of Dentistry, Thammasat University (Rangsit Campus), Pathum-thani, Thailand.
Corresponding author.
Address reprint requests to: Peng Huang, Department of Molecular Pathology, University of Texas M.D. Anderson Cancer Center, Box 0951, 1515 Holcombe Boulevard, Houston, TX 77030. E-mail:gro.nosrednadm@gnauhp
Address reprint requests to: Peng Huang, Department of Molecular Pathology, University of Texas M.D. Anderson Cancer Center, Box 0951, 1515 Holcombe Boulevard, Houston, TX 77030. E-mail:gro.nosrednadm@gnauhp
Received 2007 Oct 17; Revised 2008 Feb 6; Accepted 2008 Feb 6.

Abstract

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) play important roles in regulation of cell survival. In general, moderate levels of ROS/RNS may function as signals to promote cell proliferation and survival, whereas severe increase of ROS/RNS can induce cell death. Under physiologic conditions, the balance between generation and elimination of ROS/RNS maintains the proper function of redox-sensitive signaling proteins. Normally, the redox homeostasis ensures that the cells respond properly to endogenous and exogenous stimuli. However, when the redox homeostasis is disturbed, oxidative stress may lead to aberrant cell death and contribute to disease development. This review focuses on the roles of key transcription factors, signal-transduction pathways, and cell-death regulators in affecting cell survival, and how the redox systems regulate the functions of these molecules. The current understanding of how disturbance in redox homeostasis may affect cell death and contribute to the development of diseases such as cancer and degenerative disorders is reviewed. We also discuss how the basic knowledge on redox regulation of cell survival can be used to develop strategies for the treatment or prevention of those diseases. Antioxid. Redox Signal. 10, 1343–1374.

Abstract

Footnotes

Reviewing Editors: Junichi Sadoshima, Chandan K. Sen, Bor-Luen Tang, and Keith Webster

Footnotes

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