慢性心力衰竭（CHF）是严重危害人类健康的主要疾病之一，其机制尚未完全阐明。真武汤是CHF的有效治疗药物。前期研究发现：真武汤能够改善心肌梗死后心室重构小鼠和血管平滑肌特异性结节性硬化复合体1（TSC1）基因敲除（TSC1c/cSM22Cre+/-）小鼠的心功能、抑制其心室重构、调控心肌细胞自噬，其机制与TSC1-mTOR信号通路密切相关。基于前期研究结果，我们提出假说：真武汤通过TSC1-mTOR信号通路调控心肌细胞自噬发挥抗心室重构和CHF作用。为验证上述假说，本项目拟在TSC1c/cSM22Cre+/-小鼠基础上，通过冠状动脉左前降支结扎术制备心肌梗死后心室重构和CHF小鼠模型，利用分子生物学技术在细胞和动物水平分别观察TSC1-mTOR信号通路调控心肌细胞自噬及其在真武汤抗心室重构和CHF中的作用。本项目对进一步发掘CHF的发病机制，丰富真武汤抗CHF的疗效机理，探索一条新的途径。

Chronic heart failure (CHF) is one of the major diseases hazard to human health. However, its mechanism is not yet fully understood. Zhenwu decoction is an effective therapeutic drug for CHF. Our previous study found that: Zhenwu decoction can improve heart function, inhibit ventricular remodeling, and regulate cardiomyocytes autophagy in mice with ventricular remodeling after myocardial infarction and vascular smooth muscle cell-specific TSC1 gene knockout (TSC1c/cSM22Cre+/-) mice, and its mechanism is closely related to tuberous sclerosis complex 1 (TSC1)-mammalian target of rapamycin (mTOR) signaling pathway. Based on our previous studies, we hypothesized that: Zhenwu decoction have an effect on anti ventricular remodeling and CHF via regulating cardiomyocytes autophagy by TSC1-mTOR signaling pathway. To verify this hypothesis, this project will establish ventricular remodeling and CHF mice model by ligate the left anterior descending coronary artery causing myocardial infarction in TSC1c/cSM22Cre+/- mice, and use molecular biology techniques in cell and animal levels to observe the TSC1-mTOR signaling pathway regulating cardiomyocytes autophagy and its role in Zhenwu decoction anti ventricular remodeling and CHF. This research intend to further explore the pathogenesis of CHF, enrich the anti CHF mechanism of Zhenwu decoction, and thus to discover a new way for prevention and treatment of CHF.