CELLULAR MECHANISMS IN CARDIAC HYPERTROPHY

这项建议是对细胞和生化基础的多学科研究。 在诱导期间心脏机械性能的改变和 心肌肥厚消退。各种肥厚的动物模型将被 研究过的，包括激素(甲状腺素和异丙肾上腺素)引起的肥大 压力和体积过载。我们将集中调查 特别是在三个一般领域：1)适应性变化在 收缩蛋白在肥厚患者机械性能改变中的作用 心脏，2)引发心脏疾病的生化事件的性质 肥大和3)自主神经系统和其他 神经体液因子对代偿性心肌生长的调节作用。这个 后一领域将包括牛磺酸在不同形式的 肥大。该机构内部的调查人员将整合他们的资源， 利用常见动物模型探讨心脏疾病的基本机制 肥大。这项提议代表了合作努力的延伸。 不同的实验室已经在进行这项研究。机制一直是 为交流数据、对正在进行的研究进行批判性审查而建立的 以及对这个项目各个方面的行政控制。

This proposal is a multidisciplinary study of the cellular and biochemical basis for alterations in the mechanical performance of the heart during induction and regression of cardiac hypertrophy. Various animal models of hypertrophy will be studied, including hypertrophy induced by hormones (thyroxine and isoproterenol) and pressure and volume overload. We shall focus our investigations particularly on three general areas: 1) the role of adaptative changes in the contractile proteins in the altered mechanical performance of hypertrophied hearts, 2) the nature of the biochemical events that initiate cardiac hypertrophy and 3) the role of the autonomic nervous system and other neurohumoral factors in the modulation of compensatory myocardial growth. The latter area will include studies on the role of taurine in various forms of hypertrophy. Investigators within the institution will combine their resources, using common animal models to explore fundamental mechanisms involved in cardiac hypertrophy. This proposal represents an extension of collaborative efforts that already are underway in various laboratories. Mechanisms have been established for communication of data, critical review of research in progress and administrative control of all aspects of this project.