Nitric Oxide and the Liver

P. A. Loughran*, L. Xu, T. R. Billiar

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

2 Scopus citations


The pathological response to nitric oxide (NO) will vary in relation to the context in which NO is produced, duration, level of radical oxygen species generated and the amount of antioxidants present within the environment. The effect of NO on the primary liver cell type, hepatocytes, is controlled by the NO downstream activation of soluble guanylate cyclase and cyclic guanosine monophosphate, protein complex assembly, overexpression of stress-induced proteins or protein modification of the active site of caspase(s) by the S-nitrosative modification of cysteine. The pathophysiological roles of NO in liver will be presented with special attention of the use of experimental data generated through the use of pharmacological NO donors, inhibitors to NO generation, modulation of inflammatory cytokines, cofactor, or substrate within genetically altered knockout animals or patients when applicable.

Original languageEnglish
Title of host publicationLiver Pathophysiology
Subtitle of host publicationTherapies and Antioxidants
Number of pages18
ISBN (Electronic)9780128043219
ISBN (Print)9780128042748
StatePublished - 23 Mar 2017
Externally publishedYes


  • Apoptosis
  • Liver
  • Nitric oxide synthase
  • Nitric oxide-sGC/cGMP signaling
  • Pathobiology
  • Radical oxygen and nitrogen species
  • S-nitrosylation/denitrosation


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