Figure 1.

Cross-talk and interactions between H₂S and PKG pathways in cardiac myocytes. Exposure of cardiomyocytes to H₂S donors (or endogenously produced H₂S) leads to increased cGMP levels through activation of eNOS and/or PDE inhibition. Increased cGMP-dependent protein kinase activity results in upregulation of CSE levels and H₂S production, that further increases cGMP levels and PKG activity. Phosphorylation and inhibition of CSE by PKG serves as a brakε to control H₂S output.