MECHANISMS OF AGE ASSOCIATED CARDIAC HYPERTROPHY

据报道，在人类中，心脏质量随着年龄的增长而增加， 其他哺乳动物物种(I-9)。心肌对急性压力的反应 然而，容量超负荷的特点是新发心脏较少。 衰老心脏肥大(9-11)。我们观察到，左翼 心脏对急性血流动力学应激反应的蛋白质研究 合成、RNA合成与即刻早期基因表达(c-fos和 C-jun)与年轻成年大鼠相比，老年大鼠心脏(11)较少。我们 假设导致年龄相关心脏疾病的机制 心肌肥厚与血流动力学应激反应减弱 包括随年龄增长而改变的基因表达程序。 在五年期间，我们将检查心肌细胞的这两个变化 心肌的结构和基因表达随年龄的变化。

Cardiac mass has been reported to be increased with age in humans and other mammalian species (I-9). The myocardial response to acute pressure or volume overload, however, is characterized by less new cardiac hypertrophy in the senescent heart (9-11). We have observed that left ventricular response to acute hemodynamic stress in terms of protein synthesis, RNA synthesis and immediate early gene expression (c-fos and c-jun) are less in old compared to young adult rat hearts (11). We postulate that the mechanisms responsible for the age associated cardiac hypertrophy and the decreased myocardial response to hemodynamic stress include an altered program of gene expression that occurs with aging. During the five year period, we will examine both changes in myocardial structure and changes in myocardial gene expression as influenced by age.