心肌肥厚是心脏对应激反应的一种长期、慢性的代偿机制，导致心脏结构与功能异常。microRNA let-7家族序列保守且在心脏中表达丰富，课题组在既往研究基础上发现，心肌肥厚时let-7e-5p与-3p表达量异常且相反，即-5p表达上调，-3p表达下调。二者的异常表达是否为诱导心肌肥厚的新机制仍有待阐明。因此，我们提出假设：应激刺激时，心肌细胞内let-7e发生臂失衡：-5p表达升高，-3p表达降低，二者通过靶向不同的靶点参与心肌肥厚的调控。本项目将应用分子生物学、生物信息学等技术手段研究：（1）let-7e臂失衡是否可以调控心肌肥厚的病理进程；（2）阐明let-7e臂失衡调控心肌肥厚的分子信号通路；（3）初步探索心肌肥厚时let-7e臂失衡的发生机制。本研究将为心肌肥厚的发生、发展机制研究提供新的策略。

Cardiac hypertrophy is a long-term, chronic compensatory mechanism of heart response to stress, resulting in abnormal structure and function of heart. The microRNA let-7 family represents a conserved and abundant miRNA in the heart. Based on previous research, we found that let-7e-5p/-3p expression was abnormal and opposite during cardiac hypertrophy, that is -5p expression was up-regulated and -3p expression was down-regulated. Whether the abnormal expression of let-7e-5p/-3p is a new mechanism to induce cardiac hypertrophy remains to be elucidated. Therefore, we hypothesize that let-7e arm-imbalance was occurred in cardiomyocytes during stress stimulation, -5p expression increases and -3p expression decreases, and the two participate in the regulation of cardiac hypertrophy by targeting different targets respectively. This project will use molecular biology and bioinformatics techniques to carry out the following research: (1) whether let-7e arm-imbalance can regulate the pathological process of cardiac hypertrophy; (2) clarify the molecular signal pathway of let-7e arm-imbalance to regulate cardiac hypertrophy; (3) Initially explore the mechanism of let-7e arm-imbalance during cardiac hypertrophy. This study will provide new strategies for the study of the occurrence and development of cardiac hypertrophy.