Protein S-nitrosylation in preconditioning and postconditioning

he coronary artery disease is a leading cause of death and morbidity worldwide. This disease has a complex pathophysiology that includes multiple mechanisms. Among these is the oxidative/nitrosative stress. Paradoxically, oxidative/nitrosative signaling plays a major role in cardioprotection against ischemia/reperfusion injury. In this context, the gas transmitter nitric oxide may act through several mechanisms, such as guanylyl cyclase activation and via S-nitrosylation of proteins. The latter is a covalent modification of a protein cysteine thiol by a nitric oxide-group that generates an S-nitrosothiol. Here, we report data showing that nitric oxide and S-nitrosylation of proteins play a pivotal role not only in preconditioning but also in postconditioning cardioprotection.