The cardiac fibroblast-targeted novel strategy for diastolic heart failure

肾素-血管紧张素-醛固酮系统的激活会导致血管收缩、心肌肥厚和纤维化。已建立的动脉僵硬和心功能不全是导致慢性心力衰竭的关键因素。调节细胞内cAMP浓度是调节细胞功能最普遍的机制之一。在这项研究中，我们发现EPAC是一种由cAMP激活的交换蛋白，也是一种新的环磷酸腺苷信号效应分子，在醛固酮激活下可以抑制心肌细胞凋亡和心功能不全。刺激EPAC可能是治疗心力衰竭的一种替代策略。

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.