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.
| Original language | English |
|---|---|
| Pages (from-to) | 415-422 |
| Number of pages | 8 |
| Journal | Annals of the New York Academy of Sciences |
| Volume | 962 |
| DOIs | |
| State | Published - 2002 |
| Externally published | Yes |