S-Nitrosylation in Regulation of Inflammation and Cell Damage

Author(s): Subhajit Dasgupta*, Jenny- Jaramillo Gomez, Inderjit Singh, Mushfiquddin Khan

Journal Name: Current Drug Targets

Volume 19 , Issue 15 , 2018

  Journal Home
Translate in Chinese
Become EABM
Become Reviewer

Graphical Abstract:


Background: Cell signaling through nitric oxide (NO) is a multifaceted mechanism, which regulates metabolic activities and fate in different tissues. The peroxynitrite (ONOO-) formed as reaction product of nitric oxide radical and superoxide interacts with cell membrane phospholipids and proteins causing damage.

Objective: The reaction kinetics to form nitrotyrosine (ONOO-tyrosine) and/or nitrosylated cysteine (ONOO-cysteine) in protein molecules during posttranslational modification and nitration of lipids are therefore critical in determining cells’ signaling mechanism for survival or apoptosis.

Results: The nitrosylation was found to modulate GPCRs and activation of guanylate cyclase as well as regulate NF-κB activation. The recent findings have shown the neuroprotective effects of S- nitrosylation, though mechanism is unclear.

Conclusion: While keeping the background in mind, we address here the biological function of NO derivatives in medicine. We target four known compounds: SNAP, SIN- 1 chloride, SNP and GSNO to understand the effect of NO in different tissues. Here we analyze the existing findings to assess therapeutic relevance of NO-signaling during inflammation, vasodilation and tolerance.

Keywords: Nitric oxide, nitrosylation, G- protein coupled receptor, inflammation, neurodegeneration.

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2018
Page: [1831 - 1838]
Pages: 8
DOI: 10.2174/1389450119666180213094747
Price: $65

Article Metrics

PDF: 29