Nitric oxide (NO) is a gaseous messenger molecule synthesized from L-arginine and molecular oxygen by three different NO synthases (neuronal (n), endothelial (e), and inducible (i) NOS). Many reports suggest that excessive and abnormal production of NO plays a crucial role in neuronal cell death including neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases, as well as various conditions of vascular dysfunction. In contrast, numerous lines of evidence indicate that NO is essential for cellular function, differentiation, and survival. In general, NO can modulate cell function through signalling pathways that include the NO/cyclic guanosine monophosphate (cGMP) pathway and the S-nitrosylation pathway in which NO reversibly binds to thiol groups of proteins thereby modulating their function or through NO-associated acetylation/deacetylation or methylation/demethylation networks. In addition, NO can further modulate cell function through peroxynitrite formation leading to nitrotyrosination of protein residues, as well as through modulation of gene expression via epigenetic changes, including direct modulation of transcription factor activity. How controlled S-nitrosylation/nitrotyrosination of proteins and activation of the NO/cGMP signalling pathway promote cellular survival and induce epigenetic changes while uncontrolled signalling promotes cell death and dysfunction remains to be elucidated.

We invite investigators to contribute original research articles and review articles that address the continuing efforts to understand the molecular mechanisms underlying nitrergic signalling in vascular or neural function in healthy and diseased states. In particular, we are interested in articles describing the functional effects of posttranslational protein modifications induced by NO signalling such as S-nitrosylation or 3-nitrotyrosination.

Potential topics include, but are not limited to:

• Nitric oxide signalling at the synapse
• S-nitrosylation of cellular proteins and modulation of function
• 3-nitrotyrosination as a mediator of neurodegeneration or other neurological disorders
• Posttranslational modification by NO
• NO-mediated regulation of vascular function
• NO/NOS and arginase balance in endothelial dysfunction
• NO and regulation of gene expression/epigenetics