Abstract
Neuroinflammation is a CNS reaction to injury in which some severe pathologies, regardless of their origin, converge. The phenomenon emphasizes crosstalk between neurons and glia and reveals a complex interaction with oxidizing agents through redox sensors localized in enzymes, receptors, and transcription factors. When oxidizing pressures cause reversible molecular changes, such as minimal or transitory proinflammatory cytokine overproduction, redox couples provide a means of translating the presence of reactive oxygen or nitrogen species into useful signals in the cell. Additionally, thiol-based redox sensors convey information about localized changes in redox potential induced by physiologic or pathologic situations. They are susceptible to oxidative changes and become key events during neuroinflammation, altering the course of a signaling response or the behavior of specific transcription factors. When oxidative stress augments the pressure on the intracellular environment, the effective reduction potential of redox pairs diminishes, and cell signaling shifts toward proinflammatory and proapoptotic signals, creating a vicious cycle between oxidative stress and neuroinflammation. In addition, electrophilic compounds derived from the oxidative cascade react with key protein thiols and interfere with redox signaling. This article reviews the relevant functional aspects of redox control during the neuroinflammatory process.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 193-247 |
| Number of pages | 55 |
| Journal | Antioxidants and Redox Signaling |
| Volume | 13 |
| Issue number | 2 |
| DOIs | |
| State | Published - Jul 15 2010 |
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ASJC Scopus subject areas
- Biochemistry
- Cell Biology
- Molecular Biology
- Physiology
- Clinical Biochemistry
Cite this
Functional aspects of redox control during neuroinflammation. / Rosales-Corral, Sergio; Reiter, Russel J; Tan, Dun Xian; Ortiz, Genaro G.; Lopez-Armas, Gabriela.
In: Antioxidants and Redox Signaling, Vol. 13, No. 2, 15.07.2010, p. 193-247.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Functional aspects of redox control during neuroinflammation
AU - Rosales-Corral, Sergio
AU - Reiter, Russel J
AU - Tan, Dun Xian
AU - Ortiz, Genaro G.
AU - Lopez-Armas, Gabriela
PY - 2010/7/15
Y1 - 2010/7/15
N2 - Neuroinflammation is a CNS reaction to injury in which some severe pathologies, regardless of their origin, converge. The phenomenon emphasizes crosstalk between neurons and glia and reveals a complex interaction with oxidizing agents through redox sensors localized in enzymes, receptors, and transcription factors. When oxidizing pressures cause reversible molecular changes, such as minimal or transitory proinflammatory cytokine overproduction, redox couples provide a means of translating the presence of reactive oxygen or nitrogen species into useful signals in the cell. Additionally, thiol-based redox sensors convey information about localized changes in redox potential induced by physiologic or pathologic situations. They are susceptible to oxidative changes and become key events during neuroinflammation, altering the course of a signaling response or the behavior of specific transcription factors. When oxidative stress augments the pressure on the intracellular environment, the effective reduction potential of redox pairs diminishes, and cell signaling shifts toward proinflammatory and proapoptotic signals, creating a vicious cycle between oxidative stress and neuroinflammation. In addition, electrophilic compounds derived from the oxidative cascade react with key protein thiols and interfere with redox signaling. This article reviews the relevant functional aspects of redox control during the neuroinflammatory process.
AB - Neuroinflammation is a CNS reaction to injury in which some severe pathologies, regardless of their origin, converge. The phenomenon emphasizes crosstalk between neurons and glia and reveals a complex interaction with oxidizing agents through redox sensors localized in enzymes, receptors, and transcription factors. When oxidizing pressures cause reversible molecular changes, such as minimal or transitory proinflammatory cytokine overproduction, redox couples provide a means of translating the presence of reactive oxygen or nitrogen species into useful signals in the cell. Additionally, thiol-based redox sensors convey information about localized changes in redox potential induced by physiologic or pathologic situations. They are susceptible to oxidative changes and become key events during neuroinflammation, altering the course of a signaling response or the behavior of specific transcription factors. When oxidative stress augments the pressure on the intracellular environment, the effective reduction potential of redox pairs diminishes, and cell signaling shifts toward proinflammatory and proapoptotic signals, creating a vicious cycle between oxidative stress and neuroinflammation. In addition, electrophilic compounds derived from the oxidative cascade react with key protein thiols and interfere with redox signaling. This article reviews the relevant functional aspects of redox control during the neuroinflammatory process.
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U2 - 10.1089/ars.2009.2629
DO - 10.1089/ars.2009.2629
M3 - Article
C2 - 19951033
AN - SCOPUS:77953641852
VL - 13
SP - 193
EP - 247
JO - Antioxidants and Redox Signaling
JF - Antioxidants and Redox Signaling
SN - 1523-0864
IS - 2
ER -