形成心肌肥大，需要在心肌细胞增大时活跃地合成肌动蛋白及其他蛋白，相反地，纠正心肌肥大则需要去除心肌细胞中收缩蛋白这一重要部分。
      这一过程受到严密控制，管理这一过程的信号转导及翻译机制已被完美地描述出来。但尚未明确的是在正常及非正常心脏生物学中,这一途径被何种蛋白质转运和调节。
      通过最近的努力，我们已经明确了心脏中存在的泛素连接酶在调节心肌功能中的多种作用。这些泛素连接酶包括atrogin-1/MafBX,MURFs1-3,以及CHIP。它们以未知的方式影响蛋白质的转运、细胞信号转导以及心肌新陈代谢。在心肌细胞的功能方面，泛素连接酶的生物学性能将被总结概括，并且，其作用将会被看作为潜在的治疗目标。

Cardiac hypertrophy requires active synthesis of sarcomeric and other proteins as cardiomyocytes enlarge and, conversely, reversal of cardiac hypertrophy requires the removal of a significant fraction of contractile proteins from cardiomyocytes. These processes are tightly regulated, and the signaling and transcriptional pathways that govern them have been elegantly described. Less well known are the mechanisms by which protein turnover is regulated during normal and abnormal cardiac biology. Our recent efforts have defined multiple roles for ubiquitin ligases in the heart to regulate cardiomyocyte function. These ubiquitin ligases include atrogin-1/MafBX, MURFs1-3, and CHIP. These ubiquitin ligases affect protein turnover, cell signaling responses, and cardiac metabolism in unsuspected ways. The biology of ubiquitin ligases in the context of cardiomyocyte function will be summarized, and the roles for these ubiquitin ligases will be discussed as potential therapeutic targets.

来自第14届世界心脏病大会
张伟译 刘琳宁校