中文摘要：

心肌梗死后心室重塑是慢性心力衰竭的主要原因。因凋亡和坏死而导致的心肌细胞死亡可造成心肌重塑，病理性心肌肥大和左心室扩张是其主要特征。研究表明，泛素蛋白酶体系统（ubiquitin proteasome system，UPS）可能参与这一过程。

英文摘要：

Degradation of most proteins in eukaryotic cells is through the ubiquition - proteasome system （UPS）. Recently, it demonstrated that UPS regulates cell apoptosis and cardiac hypertrophy. The differences of UPS regulation lie in E3 ligases, which specifically recognize targets and direct the ubiquitination process. Recent evidence suggests that atrogin - 1/muscle atrophy F - box （Mafbx） and muscle RING finger 1 （ MuRF1 ） may be critical mediators of the heart and muscle atrophy and hypertrophy. This review summarizes the possible relationship between UPS and cardiac dysfunction after myocardial infarction in order to inhibit cardiac dysfunction after myocardial infarction.