Overview on Pathogenesis of Cardiac Hypertrophy
Overview on Pathogenesis of Cardiac Hypertrophy
复制标题
心脏肥大发病机制概述
作者：
M. Rabinowitz
现就可能参与心肌肥厚发病机制的一些因素作一综述。关于工作负荷增加或肌肉拉伸增加本身可能是导致心肌肥厚的刺激因素，继发于短暂的ATP耗竭的假说已经讨论过。考虑了肌原纤维和线粒体成分分别受到控制的可能性。在心肌肥厚发展的早期阶段，线粒体质量和酶活性增加，但在较长时间的压力诱导肥厚后，线粒体相对于其他心肌蛋白的质量减少。提供了显示心肌成分快速周转的数据，并强调了降解率和合成率的变化在心脏成分积累中的参与。例如，在主动脉收缩后心肌肥厚的早期阶段，线粒体细胞色素c的降解减少。实验表明，心脏蛋白质和RNA在去除狭窄的主动脉带后迅速下降，这表明心肌肥厚的消退是一个快速的过程。
Some of the factors that may be involved in the pathogenesis of cardiac hypertrophy have been reviewed. The hypotheses that transient ATP depletion secondary to increased work load or, alternatively, that increased muscle stretch itself may be the stimuli leading to cardiac hypertrophy have been discussed. The possibility that the myofibrillar and mitochondrial elements are under separate control was considered. In the earliest stages of the development of cardiac hypertrophy, mitochondrial mass and enzyme activation increase, but after longer periods of pressure-induced hypertrophy, mitochondrial mass relative to other cardiac muscle proteins decreases. Data showing the rapid turnover of myocardial components were presented, and the participation of alterations in degradation rate, as well as synthetic rate, in the accumulation of cardiac components was emphasized. For example, the degradation of mitochondrial cytochrome c is decreased during the earliest stages of cardiac hypertrophy following aortic constriction. Experiments showing that cardiac protein and RNA quickly decline after removal of a restricting aortic band indicate that regression of cardiac hypertrophy is a rapid process.