Low myocardial PKG activity contributes to increased cardiomyocyte stiffness and oxidative stress in HFPEF, suggesting it as a potential therapeutic target.
Low myocardial PKG activity in HFPEF was associated with raised cardiomyocyte F(passive) and was related to increased myocardial nitrosative/oxidative stress. The latter was probably induced by the high prevalence in HFPEF of metabolic comorbidities. Correction of myocardial PKG activity could be a target for specific HFPEF treatment.
Heerebeek et al. (Wed,) studied this question.