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Nitric oxide in liver diseases.

Yasuko Iwakiri1, Moon Young Kim2

  • 1Section of Digestive Diseases, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.

Trends in Pharmacological Sciences
|June 2, 2015
PubMed
Summary

Nitric oxide (NO) plays dual roles in liver disease. Endothelial NO synthase (eNOS)-derived NO is protective, while inducible NOS (iNOS)-derived NO is harmful, impacting liver pathogenesis.

Keywords:
eNOSendothelial cellsiNOSinflammationportal hypertension

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Area of Science:

  • Hepatology
  • Molecular Biology
  • Biochemistry

Background:

  • Nitric oxide (NO) and its derivatives are crucial in liver physiology and pathophysiology.
  • The roles of NO in liver disease are complex, with distinct effects observed based on its source.
  • Endothelial NO synthase (eNOS)-derived NO in liver sinusoidal endothelial cells (LSECs) generally protects against liver disease, whereas inducible NOS (iNOS)-derived NO contributes to pathology.

Purpose of the Study:

  • To review the multifaceted roles of NO in the development and progression of various liver diseases.
  • To highlight recent advances in understanding NO-mediated signaling pathways relevant to liver conditions.
  • To provide insights into future research directions for NO-related liver studies.

Main Methods:

  • Literature review focusing on recently published articles.
  • Analysis of the differential effects of eNOS- and iNOS-derived NO in liver disease models.
  • Examination of novel NO-mediated signaling mechanisms, including nitrated fatty acids (NO2-FAs) and S-guanylation.

Main Results:

  • eNOS-derived NO in LSECs demonstrates protective effects against liver disease pathogenesis.
  • iNOS-derived NO is implicated in promoting pathological processes in the liver.
  • Recent research has identified nitrated fatty acids (NO2-FAs) and S-guanylation as key NO-mediated signaling pathways.

Conclusions:

  • NO exhibits dichotomous roles in liver disease, with its source determining its impact.
  • Understanding NO-mediated signaling, including NO2-FAs and S-guanylation, is critical for deciphering liver disease mechanisms.
  • Further research is warranted to explore therapeutic strategies targeting NO pathways in liver diseases.