The Role of Nitric Oxide in Apoptosis and Autophagy: Biochemical and Computational Studies

摘要: Publisher Summary This chapter focuses on the regulation and function of nitric oxide (NO)/inducible NOS (iNOS) in liver settings acute inflammation. It also helps understanding factors that govern consequence sustained NO production tissues investigates mechanisms cytotoxicity, such as necrosis autophagy. In liver, iNOS limits cell death endotoxemia, regeneration, exposure to ligands, while conversely creating hepatic damage under ischemia/reperfusion hemorrhagic shock. Organ physiology pathophysiological response (NO) vary across a range inflammatory stresses trauma, hemorrhage, injury, sepsis, part reflected by amount, duration, type, source NO. The is primary site stress, which generated inducible synthase may impact cell/tissue/organ either positively or negatively. These divergent outcomes appear depend context milieu produced, including levels antioxidants generation reactive oxygen species, trigger protection death. Specifically, fate hepatocyte, controlled downstream activation soluble guanylate cyclase cyclic guanosine monophosphate, S-nitrosative inhibition active cysteine within enzymes architect apoptosis, caspases. can modulate complex variety processes signaling, modification proteins, gene expression affect apoptosis related process autophagy cell-specific manner. switch between positive negative cells, tissues, organs will be discussed with special attention use experimental data mathematical models identify likely actions future therapeutic directions.