title: Mechanisms of hepatoprotection by nitric oxide.
abstract: Nitric oxide (NO) exerts numerous antiapoptotic effects on hepatocytes in settings of inflammation and tissue damage. These actions of NO are modulated by a variety of mechanisms under both physiologic and pathologic conditions. Nitric oxide inhibits cell death or apoptosis by modulation of heat shock proteins, S-nitrosylation of caspases at their catalytic site cysteine residue, triggering of the cGMP pathway, and prevention of mitochondrial dysfunction. Our preliminary studies also suggest that NO can modulate apoptosis-related genes in a manner consistent with an antiapoptotic effect. This review focuses on these molecular mechanisms of cytoprotection by NO.
authors.affiliation: Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
authors.forename: Yinna
authors.initials: Y
authors.lastname: Wang
authors.forename: Yoram
authors.initials: Y
authors.lastname: Vodovotz
authors.forename: Peter K M
authors.initials: PK
authors.lastname: Kim
authors.forename: Ruben
authors.initials: R
authors.lastname: Zamora
authors.forename: Timothy R
authors.initials: TR
authors.lastname: Billiar
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D020169:Caspases / Q000378:metabolism; D019610:Cytoprotection / Q000502:physiology*; D006360:Heat-Shock Proteins / Q000378:metabolism; D022781:Hepatocytes / Q000187:drug effects*; D008928:Mitochondria / Q000187:drug effects; D009569:Nitric Oxide / Q000494:pharmacology*; D015398:Signal Transduction / Q000502:physiology
chemical_list: D006360:Heat-Shock Proteins; D009569:Nitric Oxide; D020169:Caspases