CELLULAR MECHANISMS IN CARDIAC HYPERTROPHY

心脏肥大的细胞机制

• 批准号: 3097780
• 负责人: EUGENE MORKIN
• 金额: $ 73.31万
• 依托单位: UNIVERSITY OF ARIZONA
• 依托单位国家: 美国
• 财政年份: 1977
• 资助国家: 美国
• 起止时间: 1977-09-01 至 1988-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3097780
• 关键词: cellular pathology; heart enlargement; heart failure; muscle proteins

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.

这个建议是一个多学科的研究细胞和生化基础 诱导期间心脏机械性能的改变， 心脏肥大的消退。 将研究各种肥大的动物模型。 研究，包括激素（甲状腺素和异丙肾上腺素）诱导的肥大 以及压力和容量过载。 我们将集中调查 特别是在三个一般领域：1）适应性变化的作用 收缩蛋白在肥大细胞机械性能改变中的作用 心脏，2）启动心脏的生化事件的性质 肥大和3）自主神经系统和其他的作用 神经体液因子在心肌代偿性生长调节中的作用 的 后一领域将包括研究牛磺酸在各种形式的 肥厚 机构内的调查人员将联合收割机整合他们的资源， 使用常见的动物模型来探索心脏的基本机制， 肥厚 这一提议是合作努力的延伸 已经在不同的实验室中进行。 机制已经 为交流数据、对正在进行的研究进行严格审查而设立 和行政控制的各个方面。