Of interest, it has been reported in an experimental model of prediabetes in young rats that mitochondrial oxidative stress in cardiomyocytes contributes to the depression of soluble guanylyl cyclase/PKG activity and impairment of relaxation with subsequent diastolic dysfunction, which preceded the coronary endothelial dysfunction (indicated by preservation of the dilator response to acetylcholine in microcirculation) [31]. Here, PRKG1 is linked to prediabetes syndrome.