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S-nitrosothiol signaling regulates liver development and improves outcome following toxic liver injury

Andrew G Cox1, Diane C Saunders1, Peter B Kelsey1

  • 1Genetics Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Cell Reports
|January 7, 2014
PubMed

Insights

Toxic liver injury can be treated by targeting S-nitrosoglutathione reductase (GSNOR). Inhibiting GSNOR protects the liver from damage, promotes regeneration, and improves survival, offering new therapeutic options.

Area of Science:

  • Hepatology
  • Toxicology
  • Biochemistry

Background:

  • Toxic liver injury is a major cause of liver failure with limited treatment options.
  • Understanding the mechanisms of liver damage protection and repair is crucial.
  • S-nitrosothiols are identified as key regulators of liver growth and injury response.

Purpose of the Study:

  • To investigate the role of S-nitrosothiols in liver regeneration and protection from toxic injury.
  • To evaluate the therapeutic potential of targeting S-nitrosoglutathione reductase (GSNOR) in liver injury models.

Main Methods:

  • Studies in zebrafish demonstrated nitric oxide's role in liver formation.
  • Acetaminophen (APAP) induced liver injury model in GSNOR-deficient mice.
  • Administration of a GSNOR-specific inhibitor and N-acetylcysteine (NAC) in preclinical models.

Main Results:

  • Inhibition of GSNOR minimized APAP-induced liver damage and enhanced survival.
  • GSNOR inhibition sustained activation of the cytoprotective Nrf2 pathway.
  • GSNOR inhibitors improved liver histology and expanded the therapeutic window when combined with NAC.

Conclusions:

  • S-nitrosothiol signaling, regulated by GSNOR, plays a vital role in liver protection and repair across vertebrates.
  • GSNOR inhibitors represent promising therapeutic candidates for treating toxic liver injury.
  • Targeting GSNOR offers a novel strategy to improve outcomes in liver failure patients.

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