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. Author manuscript; available in PMC: 2024 Aug 1.
Published in final edited form as: Cardiovasc Drugs Ther. 2021 Oct 15;37(4):793–806. doi: 10.1007/s10557-021-07275-y

Figure 1.

Figure 1

Effect of phosphodiesterase-5 inhibitors in cardiovascular disease. Schematic summary of the proposed mechanisms by which phosphodiesterase-5 inhibitors exert their cardioprotective effect. The PKG-mediated suppression of calcineurin, leading to suppression of cardiomyocyte hypertrophy, and PKG-mediated phosphorylation of phospholamban at Ser16, leading to restored SERCA activity, are parallel events. Redox signals from mitochondria with activated mitochondrial Katp channels lead to phosphorylation of GSK-3beta-Ser9, which inhibits opening of mitochondrial permeability transition pores, protecting against necrosis. cGMP, cyclic guanosine monophosphate; eNOS, endothelial nitric oxide synthase; ERK, extracellular signal-regulated kinases; GC, guanylate cyclase; GSK3ß-Ser9, glycogen synthase kinase 3 beta serine 9; HF, heart failure; iNOS, inducible nitric oxide synthase; LV, left ventricle; LVEDD, left ventricular end diastolic diameter; LVH, left ventricular hypertrophy; mitochondrial KATP, mitochondrial ATP-sensitive potassium; NGF, nerve growth factor; NO, nitric oxide; PDE5, phosphodiesterase-5; PKG, protein kinase G; SERCA, sarcoplasmic reticulum calcium ATPase