心肌能量代谢异常能够导致心室重构，但具体机制不明。研究发现AMPK/mTOR 信号通路是细胞能量合成/分解代谢的开关，该通路能够通过介导心肌细胞自噬引起心室重构。前期研究显示养心康能够改善心室重构，影响AMP/ATP比值，调控心肌自噬水平，而AMP/ATP比值升高是激活AMPK的重要因素。据此我们推测养心康改善心室重构的机制可能是通过调节心肌细胞能量代谢，干预AMPK/mTOR信号通路调控心肌细胞自噬水平而实现的。本项目拟观察衰竭心肌的能量代谢规律，通过特异性激活或抑制AMPK/mTOR通路，以自噬体超微结构及自噬体膜蛋白标志物为观察载体系统，阐明心肌能量代谢异常在心室重构发展中的作用及分子机制；在养心康干预下，通过在体和离体实验，观察养心康对心肌能量代谢、AMPK/mTOR信号通路、心肌细胞自噬和心室重构的影响，在整体、器官、细胞及分子水平上阐明养心康防治心室重构的作用机制。

Myocardial energy metabolism abnormality can lead to ventricular remodeling, but its specific mechanism is still unknown.The research have found that AMPK/mTOR signal pathway acting as a switch between cell energy catabolism and anabolism, which can lead to ventricular remodeling mediated by autophagy in myocardial cells. Early studies have shown Yangxinkang can improve ventricular remodeling，affect the AMP/ATP ratio, regulate myocardial autophagy level, and increasing ratio of AMP/ATP ,which is an important factor in the activation of AMPK. Accordingly, we speculated that the Yangxinkang can improve ventricular remodeling mechanism may be through the regulation of myocardial cell energy metabolism, intervention AMPK/mTOR signal pathway, regulation the level of myocardial autophagy. This study is to observe the regularity of failure myocardial energy metabolism, to clarify the function and the molecular mechanism of myocardial energy metabolism abnormality in ventricular remodeling through specific activation or inhibition of AMPK-mTOR pathway, with ultrastructure of autophagosome and autophagic membrane protein markers as the vector observation system；With the intervention of Yangxinkang, through in-vivo and in-vitro experiments to observe the impact of Yangxinkang on myocardial energy metabolism AMPK/mTOR signal pathway, cardiac autophagy and ventricular remodeling.In the whole, organ, cell and molecular level,to clarify the mechanism of preventing ventricular remodeling by Yangxinkang .