Characterization of mice with a deletion of protein kinase G type I in cardiomyocytes and the effect on cardioprotection through either postconditioning or mitochondria-targeted S-nitrosothiol

Objective We developed mice with a cardiomyocyte-specific ablation of the cGKI gene (CMG-KO) and tested whether protection against reperfusion injury by ischemic postconditioning (IPost), soluble guanylyl cyclase (sGC) activation, the adenosine A2B receptor (A2BAR), or the mitochondria-targeted S-nitrosothiol (MitoSNO) was affected. MitoSNO accumulates within mitochondria, driven by the membrane potential, where it generates NO and S-nitrosated thiol proteins [1].