线粒体功能障碍与心肌肥厚的发生机制

Role of mitochondrial dysfunction in myocardial hypertrophy

心肌肥厚是心脏对本身超载做出的适应性反应,适度的肥厚能保持心脏功能,但持久的肥厚终究会致使心力衰竭,探究心肌肥厚的发病机制对防止恶化为心力衰竭有重要意义.线粒体是有氧呼吸的主要场所,不仅提供细胞生存所必需的能量,还介导细胞分化、信息传递和细胞凋亡等,线粒体出现任何异常改变都会影响细胞的存活.由于心肌细胞线粒体密度高,且心肌收缩完全依赖于线粒体氧化磷酸化产生的ATP,因此心脏组织的病理改变往往与线粒体代谢及功能密切相关.越来越多的研究证明线粒体形态和功能异常是心肌肥厚发生发展的重要机制,本文就线粒体功能障碍作为心肌肥厚的发病机制作一综述.

The adaptive response of the heart to its own overload is characteristic of cardiac hypertrophy. Moderate hypertrophy can maintain cardiac efficacy but persistent hypertrophy will eventually lead to heart failure. To explore the pathogenesis of myocardial hypertrophy is of great significance to prevent the deterioration of heart failure. Aerobic respiration takes place mainly in mitochondria that not only provide energy necessary for cell survival, but also mediate cell differentiation, information transmission and apoptosis. Any abnormal changes in mitochondria will directly determine cell survival. Because of the high density of mitochondria in cardiac myocytes and the complete dependence of myocardial contraction on ATP generated by mitochondrial oxidative phosphorylation, the pathological changes of cardiac tissue are often closely related to mitochondrial metabolism and function. A growing number of studies have proved that abnormal mitochondrial morphology and function are important mechanisms for the occurrence of myocardial hypertrophy. This article discusses mitochondrial dysfunction as the pathogenesis of myocardial hypertrophy.