Nitric oxide signaling and nitrosative stress in neurons: Role for S-nitrosylation

Neelam Shahani, Akira Sawa

Research output: Contribution to journalReview articlepeer-review

60 Scopus citations


Nitric oxide (NO) mediates cellular signaling pathways that regulate a plethora of physiological processes. One of the signaling mechanisms mediated by NO is through S-nitrosylation of cysteine residues in target proteins, which is now regarded as an important redox-based physiological action. Deregulation of the protein S-nitrosylation upon nitrosative stress, however, has also been linked to various human diseases, such as neurodegenerative disorders. Between these physiological and pathophysiological roles, there are mechanisms whereby a milder level of nitrosative stress provides S-nitrosylation of some proteins that counteracts the pathological processes, serving as a negative feedback mechanism. In addition, NO has recently emerged as a mediator of epigenetic gene expression and chromatin changes. In this review, these molecular mechanisms, especially those in the central nervous system and neurodegenerative disorders, are described.

Original languageEnglish (US)
Pages (from-to)1493-1504
Number of pages12
JournalAntioxidants and Redox Signaling
Issue number8
StatePublished - Apr 15 2011

ASJC Scopus subject areas

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


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