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Background Phosphodiesterase (PDE) 5 inhibitors, which prevent cGMP degradation and therefore elevate its level in the heart, have been shown to protect the myocardium in several animal models of heart failure and in human trials. cGMP binding to protein kinase G (PKG) results in its classical activation and also prevents disulfide dimerisation-dependent activation of this kinase. Doxorubicin (DOX) is an anti-cancer drug which commonly causes cardiomyopathy, the pathogenesis of which is associated with increased oxidant production and apoptosis. We hypothesised that oxidative activation of PKG Ia may mediate DOX-induced cardiotoxicity, and PDE5 inhibitors may be protective because they elevate cGMP which then limits the oxidative activation.

Tadalafil protects from doxorubicin-induced heart failure by attenuating PKG Iα disulfide dimerisation