线粒体之间的信号和物质交换对于维持线粒体群体均一性和正常线粒体功能至关重要。心肌细胞内线粒体含量丰富，排列有序，线粒体运动极不活跃。对心肌细胞中线粒体动态改变及线粒体间通讯的研究较少。我们近期发现心肌细胞线粒体之间通过两种新的通讯方式-线粒体吻合和纳米通道进行物质交换，使整个心肌细胞的线粒体形成一个动态的连续功能网络，从而维持心肌细胞功能完整性。本课题将在前期研究基础上，采用生物信息学和分子遗传学手段，通过激光共聚焦显微镜生物成像技术，筛查心肌细胞线粒体吻合和纳米通道的关键调控分子，明确其调控线粒体通讯的作用机制；结合整体心肌肥厚心衰病理动物模型，阐明线粒体通讯的关键调控分子在病理情况下的变化规律和调控机制，从而了解线粒体通讯的病理生理意义，为线粒体功能障碍相关心脏疾病的基础和临床研究提供新的切入点和干预靶点。

Mitochondrial communication plays pivotal roles in maintaining mitochondrial health and regulating mitochondrial functions. Dysfunction of mitochondrial communication has been implicated in cardiac diseases, such as cardiac hypertrophy, ischemia/reperfusion injury, and heart failure. However, there is no direct evidence showing that cardiac mitochondria communicate with each other. In our recently published study, we has visualized two novel forms of cardiac mitochondrial communication, mitochondrial kissing and nanotunneling. Through kissing and nanotunneling, the whole population of mitochondria in a cardiomyocyte forms one dynamically continuous network. In the present study, we will identify the molecular entities of mitochondrial kissing and nanotunneling, reveal the underlying mechanisms of inter-mitochondrial communication. Moreover, with the combination of cardiac hypertrophy and heart failure rat models, we will try to understand the pathophysiological relevance of inter-mitochondrial communication in the heart. Our findings may eventually lead to the development of new treatments for mitochondrial dysfunction-related cardiac diseases, including cardiac hypertrophy, myocardial infarction and heart failure.