Functional aspects of redox control during neuroinflammation

Sergio Rosales-Corral, Russel J. Reiter, Dun Xian Tan, Genaro G. Ortiz, Gabriela Lopez-Armas

Research output: Contribution to journalReview articlepeer-review

60 Scopus citations


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 languageEnglish (US)
Pages (from-to)193-247
Number of pages55
JournalAntioxidants and Redox Signaling
Issue number2
StatePublished - Jul 15 2010

ASJC Scopus subject areas

  • Molecular Biology
  • Biochemistry
  • Physiology
  • Clinical Biochemistry
  • Cell Biology


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