Nitrite mediates cytoprotection after ischemia/reperfusion by modulating mitochondrial function

摘要: Nitrite, once thought to be an inert biomarker of NO formation, is now recognized as endocrine storage pool bioactive NO. While nitrite mediates a number hypoxic responses, one its most robust effects ability confer cytoprotection after ischemia/reperfusion in organs and models. The mechanism this appears mediated at the level mitochondrion. Here we review studies demonstrating that cytoprotective heart describe cytoprotection, which involves post-translational modification complex I leading modulation mitochondrial reactive oxygen species generation reperfusion. nitrite-dependent will compared other agents including ischemic preconditioning.