The cardiac fibroblast-targeted novel strategy for diastolic heart failure

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Activation of the renin-angiotensin-aldosterone system results in vasoconstriction, cardiac hypertrophy and fibrosis. Established arterial stiffness and cardiac dysfunction are key factors contributing to chronic heart failure. Regulation of intracellular concentrations of cyclic AMP is one of the most ubiquitous mechanisms for regulating cellular functions. In this study we showed Epac, an exchange protein activated by cAMP and a new effector molecule of cyclic AMP signaling, inhibited myocardial apoptosis and cardiac dysfunction under activation of aldosterone. Stimulation of Epac may be an alternative strategy for heart failure.